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PubMed1992

Narcolepsy: pathogenesis and nursing care.

Narcolepsy is a chronic, incurable disorder affecting at least a quarter of a million Americans. It is characterized by a tetrad of symptoms, which include excessive daytime sleepiness, cataplexy, sleep paralysis and hypnogogic hallucinations. Individuals may experience severe negative psychosocial consequences associated with these symptoms. The neuropathology of narcolepsy is largely unknown. Current work implicates decreased production or utilization of norepinephrine, dopamine and serotonin in the brain, and excessively numerous or hypersensitive cholinergic receptors in the brain. Medical management includes the use of separate drug therapies to control sleep attacks and cataplectic episodes. Nursing management requires comprehensive assessment of the interplay between the patient and environment and assistance with long-term coping.

Amphetamines↗
PubMedDate not supplied

[New perspectives in the diagnosis and therapy of narcolepsy].

Narcolepsy syndrome is a common, although often misdiagnosed, neurological disorder, whose clinical features are excessive daytime somnolence with sleep attacks, caplexy, sleep paralysis and hypnagogic hallucinations. The clinical manifestation have been interpreted as the expression of a sudden intrusion of dissociated REM phenomena in wakefulness. Sometimes the clinical manifestations may include only some of the symptoms: in particular, the cases in which the only symptom is excessive daytime somnolence may be difficult to diagnose. The etiopathogenesis of narcolepsy syndrome is still poorly understood. Recent experimental evidences suggest that a protein, called "orexin", which is supposed to play a role in the control mechanisms of both sleep and eating behaviour, is involved in its pathogenesis. The treatment of narcolepsy has been, up to now, exclusively symptomatic, and in some way empirical and unsatisfactory, especially regarding to daytime sleepiness. Recently, new pharmacological agents, acting on the serotoninergic and/or noradrenergic systems, allow a better control of the cataplectic attacks. The recent development of modafinil, a central nervous system stimulant, devoid of the serious side effects of amphetamines and other compounds, allows to hope in a better control of daytime somnolence and sleep attacks. The aim of the paper is to describe the recent advances in the diagnosis and treatment of narcolepsy.

Catalepsy↗
PubMed2003

The narcoleptic borderland: a multimodal diagnostic approach including cerebrospinal fluid levels of hypocretin-1 (orexin A).

OBJECTIVES: Biological markers of narcolepsy with cataplexy (classical narcolepsy) include sleep-onset REM periods (SOREM) on multiple sleep latency tests (MSLT), HLA-DQB1*0602 positivity, low levels of cerebrospinal fluid (CSF) hypocretin-1 (orexin A), increased body mass index (BMI), and high levels of CSF leptin. The clinical borderland of narcolepsy and the diagnostic value of different markers of narcolepsy remain controversial and were assessed in a consecutive series of 27 patients with hypersomnia of (mainly) neurological origin. METHODS: Diagnoses included classical narcolepsy (n=3), symptomatic narcolepsy (n=1), narcolepsy without cataplexy (n=4), idiopathic hypersomnia (n=5), hypersomnia associated with psychiatric disorders (n=5), and hypersomnia secondary to neurological disorders or of undetermined origin (n=9). Clinical assessment included BMI, Epworth Sleepiness Scale (ESS), Ullanlinna Narcolepsy Scale (UNS), and history of REM-symptoms (sleep paralysis, hallucinations). HLA-typing, electrophysiological studies (conventional polysomnography, MSLT, 1-week actigraphy), and measurements of CSF levels of hypocretin and leptin were also performed. RESULTS: Hypocretin-1 was undetectable in three patients with classic narcolepsy and detectable in the remaining 24 patients. Other narcoleptic markers also frequently found in patients without narcolepsy included ESS>14 (78% of 27 patients), UNS>14 (75%), REM symptoms (30%), sleep latencies on MSLT<5 min (41%), >/=2 SOREM (30%), DQB1*0602 positivity (52%), BMI>25 (52%), and increased CSF leptin (48%). Hypersomnia was documented by an increased time 'asleep' in 41% of patients. Overlapping clinical and electrophysiological findings were seen mostly in patients with narcolepsy without cataplexy, idiopathic hypersomnia, and psychiatric hypersomnia. CONCLUSIONS: (1) Hypocretin dysfunction is not the 'final common pathway' in the pathophysiology of most hypersomnolent syndromes that fall on the borderline for a diagnosis of narcolepsy. (2) The observed overlap among these hypersomnolent syndromes implies that current diagnostic categories are not entirely unambiguous. (3) A common hypothalamic, hypocretin-independent dysfunction may be present in some of these syndromes.

Adolescent↗
PubMed1994

Practice parameters for the use of stimulants in the treatment of narcolepsy. Standards of Practice Committee of the American Sleep Disorders Association.

Narcolepsy is a disorder of the central nervous system characterized by excessive sleepiness, cataplexy, and other rapid-eye-movement (REM)-sleep phenomena such as sleep paralysis and hypnagogic hallucinations. Although stimulants are the only effective treatment for the sleepiness of narcolepsy, no clinical guidelines on the use of stimulants in the treatment of narcolepsy have been published that address the following factors: appropriate doses; development of tolerance; potential for side effects, adverse reactions and abuse; and use in children and pregnant or breast-feeding women. These practice parameters from the American Sleep Disorders Association provide the first clinical guidelines on the appropriate use of stimulants in the treatment of narcolepsy.

Adolescent↗
PubMed2001

Current concepts in the etiology, diagnosis and treatment of narcolepsy.

Background and purpose: Narcolepsy is the most common neurologic cause of excessive daytime sleepiness. Rapid eye movement (REM) sleep phenomena such as cataplexy, sleep paralysis and hypnagogic hallucinations can also occur. Cataplexy, a sudden bilateral loss of muscle tone usually brought on by emotional reactions such as excitement, is essentially unique to narcolepsy. Narcolepsy, which has a prevalence of 0.02-0.05% in the US, has a profound influence on the quality of life and safety of affected individuals.Patients and methods: The most characteristic and striking physiological abnormality observed in narcolepsy is the sleep-onset REM, or the occurrence of REM sleep at, or within 20 min of, the onset of sleep. The diagnosis is established by nocturnal polysomnography, and the Multiple Sleep Latency Test (MSLT).Results: Familial cases of narcolepsy have been reported, with the risk to first-degree relatives estimated at 1-2%; however, most cases are sporadic and the syndrome is generally believed to involve environmental factors acting on a specific genetic background. The observation of an HLA association in narcolepsy suggests that autoimmunity may play a role in the disorder. However, extensive studies have failed to find convincing evidence of an autoimmune process. Patients with narcolepsy have recently been shown to be deficient in hypocretin, also called orexin, in the cerebrospinal fluid and have a reduction in hypocretin cells in the lateral hypothalamus. This suggests that hypocretins could potentially provide a novel therapeutic approach to the treatment of narcolepsy.Conclusions: Although non-pharmacologic measures can be helpful in treating narcolepsy, most patients require pharmacotherapy that includes psychostimulants or modafinil. Cataplexy is controlled by tricyclic antidepressants or selective serotonin reuptake inhibitors.

Journal Article↗
PubMed2003

Narcolepsy: differential diagnosis or etiology in some cases of bipolar disorder and schizophrenia?

Does narcolepsy, a neurological disease, need to be considered when diagnosing major mental illness? Clinicians have reported cases of narcolepsy with prominent hypnagogic hallucinations that were mistakenly diagnosed as schizophrenia. In some bipolar disorder patients with narcolepsy, the HH resulted in their receiving a more severe diagnosis (ie, bipolar disorder with psychotic features or schizoaffective disorder). The role of narcolepsy in psychiatric patients has remained obscure and problematic, and it may be more prevalent than commonly believed. Classical narcolepsy patients display the clinical "tetrad"--cataplexy, hypnagogic hallucinations, daytime sleep attacks, and sleep paralysis. Over 85% also display the human leukocyte antigen marker DQB1*0602 (subset of DQ6). Since 1998, discoveries in neuroanatomy and neurophysiology have greatly advanced the understanding of narcolepsy, which involves a nearly total loss of the recently discovered orexin/hypocretin (hypocretin) neurons of the hypothalamus, likely by an autoimmune mechanism. Hypocretin neurons normally supply excitatory signals to brainstem nuclei producing norepinephrine, serotonin, histamine, and dopamine, with resultant suppression of sleep. They also project to basal forebrain areas and cortex. A literature review regarding the differential diagnosis of narcolepsy, affective disorder, and schizophrenia is presented. Furthermore, it is now possible to rule out classical narcolepsy in difficult psychiatric cases. Surprisingly, psychotic patients with narcolepsy will likely require stimulants to fully recover. Many conventional antipsychotic drugs would worsen their symptoms and make them appear to become a "chronic psychotic," while in fact they can now be properly diagnosed and treated.

Bipolar Disorder↗
PubMed2005

Symptomatic narcolepsy, cataplexy and hypersomnia, and their implications in the hypothalamic hypocretin/orexin system.

Human narcolepsy is a chronic sleep disorder affecting 1:2000 individuals. The disease is characterized by excessive daytime sleepiness, cataplexy and other abnormal manifestations of REM sleep, such as sleep paralysis and hypnagogic hallucinations. Recently, it was discovered that the pathophysiology of (idiopathic) narcolepsy-cataplexy is linked to hypocretin ligand deficiency in the brain and cerebrospinal fluid (CSF), as well as the positivity of the human leukocyte antigen (HLA) DR2/DQ6 (DQB1*0602). The symptoms of narcolepsy can also occur during the course of other neurological conditions (i.e. symptomatic narcolepsy). We define symptomatic narcolepsy as those cases that meet the International Sleep Disorders Narcolepsy Criteria, and which are also associated with a significant underlying neurological disorder that accounts for excessive daytime sleepiness (EDS) and temporal associations. To date, we have counted 116 symptomatic cases of narcolepsy reported in literature. As, several authors previously reported, inherited disorders (n=38), tumors (n=33), and head trauma (n=19) are the three most frequent causes for symptomatic narcolepsy. Of the 116 cases, 10 are associated with multiple sclerosis, one case of acute disseminated encephalomyelitis, and relatively rare cases were reported with vascular disorders (n=6), encephalitis (n=4) and degeneration (n=1), and hererodegenerative disorder (three cases in a family). EDS without cataplexy or any REM sleep abnormalities is also often associated with these neurological conditions, and defined as symptomatic cases of EDS. Although it is difficult to rule out the comorbidity of idiopathic narcolepsy in some cases, review of the literature reveals numerous unquestionable cases of symptomatic narcolepsy. These include cases with HLA negative and/or late onset, and cases in which the occurrences of the narcoleptic symptoms are parallel with the rise and fall of the causative disease. A review of these cases (especially those with brain tumors), illustrates a clear picture that the hypothalamus is most often involved. Several cases of symptomatic cataplexy (without EDS) were also reported and in contrast, these cases appear to be often associated with non-hypothalamic structures. CSF hypocretin-1 measurement were also carried out in a limited number of symptomatic cases of narcolepsy/EDS, including narcolepsy/EDS associated with tumors (n=5), head trauma (n=3), vascular disorders (n=5), encephalopathies (n=3), degeneration (n=30), demyelinating disorder (n=7), genetic/congenital disorders (n=11) and others (n=2). Reduced CSF hypocretin-1 levels were seen in most symptomatic narcolepsy cases of EDS with various etiologies and EDS in these cases is sometimes reversible with an improvement of the causative neurological disorder and an improvement of the hypocretin status. It is also noted that some symptomatic EDS cases (with Parkinson diseases and the thalamic infarction) appeared, but they are not linked with hypocretin ligand deficiency. In contrast to idiopathic narcolepsy cases, an occurrence of cataplexy is not tightly associated with hypocretin ligand deficiency in symptomatic cases. Since CSF hypocretin measures are still experimental, cases with sleep abnormalities/cataplexy are habitually selected for CSF hypocretin measures. Therefore, it is still not known whether all or a large majority of cases with low CSF hypocretin-1 levels with CNS interventions, exhibit EDS/cataplexy. It appears that further studies of the involvement of the hypocretin system in symptomatic narcolepsy and EDS are helpful to understand the pathophysiological mechanisms for the occurrence of EDS and cataplexy.

Child↗
PubMed1997

Pharmacological aspects of human and canine narcolepsy.

Narcolepsy-cataplexy is a disabling neurological disorder that affects 1/2000 individuals. The main clinical features of narcolepsy, excessive daytime sleepiness and symptoms of abnormal REM sleep (cataplexy, sleep paralysis, hypnagogic hallucinations) are currently treated using amphetamine-like compounds or modafinil and antidepressants. Pharmacological research in the area is facilitated greatly by the existence of a canine model of the disorder. The mode of action of these compounds involves presynaptic activation of adrenergic transmission for the anticataplectic effects of antidepressant compounds and presynaptic activation of dopaminergic transmission for the EEG arousal effects of amphetamine-like stimulants. The mode of action of modafmil is still uncertain, and other neurochemical systems may offer interesting avenues for therapeutic development. Pharmacological and physiological studies using the canine model have identified primary neurochemical and neuroanatomical systems that underlie the expression of abnormal REM sleep and excessive sleepiness in narcolepsy. These involve mostly the pontine and basal forebrain cholinergic, the pontine adrenergic and the mesolimbic and mesocortical dopaminergic systems. These studies confirm a continuing need for basic research in both human and canine narcolepsy, and new treatments that act directly at the level of the primary defect in narcolepsy might be forthcoming.

Animals↗
PubMed1999

Anesthesia considerations for patients with narcolepsy.

Narcolepsy is a derangement of the normal sleep-wakefulness rhythms. Originally, narcolepsy was thought to be a form of epilepsy; however, with the development and subsequent refinement of the electroencephalograph, this notion is no longer accepted. The disorder is characterized by inappropriate intrusions of rapid eye movement sleep into the wakeful state and multiple disruptions of the sleep cycles. Narcolepsy usually has its onset anytime between the ages of 10 years and 50 years, with the greatest majority of patients first reporting noticeable symptoms between the ages of 15 and 35 years. Patients with narcolepsy may exhibit excessive daytime sleepiness, cataplexy, hypnogogic and/or hypnopompic hallucinations, and sleep paralysis. The cause of narcolepsy is presently unknown. Recent research has identified a possible genetic contribution via chromosome 6, but some form of environmental influence appears to be necessary for the disorder to be manifested. There is no cure for narcolepsy; however, symptomatic relief may be achieved through a trial-and-error combination of amphetamines and tricyclic antidepressants. The nature of narcolepsy often forces the individual to undergo some rather dramatic lifestyle changes and can lead to the development of other associate disorders, such as depression and obesity.

Anesthesia↗
PubMedDate not supplied

A clinical picture of child and adolescent narcolepsy.

Although narcolepsy is rarely diagnosed before adulthood, symptoms often begin much earlier and can easily mimic psychiatric disorders in children and adolescents. Clinical experience from a pediatric sleep center is reviewed in 16 consecutive cases of polysomnographically proven narcolepsy with onset of symptoms by age 13 years. Only 1 of the 16 patients presented with the classic clinical tetrad of symptoms (sleepiness, cataplexy, hypnagogic hallucinations, and sleep paralysis). Behavioral and emotional disturbances were present in 12 of 16 cases, with four patients appearing to have been misdiagnosed with a psychiatric disorder before recognition of the narcolepsy. Obesity appeared as an unexpected association in this case series, with 11 of the 16 narcoleptic patients found to be overweight at the time of diagnosis. The varied clinical presentations, polysomnographic findings, family history, and associated psychiatric symptoms are described. The importance of considering narcolepsy in the differential diagnosis of any child or adolescent with excessive sleepiness is emphasized.

Adolescent↗
PubMed2005

The association between narcolepsy and REM behavior disorder (RBD).

BACKGROUND AND PURPOSE: Rapid eye movement (REM) sleep Behavior Disorder (RBD) is a movement disorder associated with loss of REM-related muscle atonia and is characterized by complex, vigorous and frequently violent dream-enacting behavior during REM sleep. RBD is usually idiopathic or secondary to neurological problems such as Parkinson's disease. This study looked at the association of RBD with another sleep disorder, narcolepsy. PATIENTS AND METHODS: Seventy-eight questionnaires were sent to known narcoleptics chosen at random from those with contact details available at the center. The questionnaire addressed current narcolepsy symptoms, medication use and symptoms of RBD. Positive questionnaire results were followed up with a telephone interview. Limited polysomnography (PSG) data was also analyzed. RESULTS: Fifty-five patients responded (response rate 71%). Of these, 20 (36%) had symptoms suggestive of RBD. The typical RBD patient is an older male (mean age of onset 60.9 years, 87% male); however, in this study, females were as likely to have RBD as males, and the mean age was 41 years. Sixty-eight percent of patients who regularly experienced cataplexy and the associated symptoms of narcolepsy (sleep paralysis, hypnogogic hallucinations and automatic behavior) had RBD, compared to 14% of those who never or rarely experienced these symptoms. CONCLUSION: This study implies a stronger relationship between these disorders than a previously published figure of 7-12% This is clinically significant as RBD is a potentially distressing but readily treatable disorder. It follows that narcoleptics, especially those with cataplexy and other associated symptoms, should be questioned about symptoms of RBD and treated accordingly. Similarly, anyone presenting with RBD should be assessed for symptoms of narcolepsy, particularly if female or of a younger age group than would otherwise be expected.

Adolescent↗
PubMed2002

Severity of narcolepsy among French of different ethnic origins (south of France and Martinique).

STUDY OBJECTIVES: The aim of the study was to describe the clinical and polygraphical characteristics of narcoleptics, with and without cataplexy and to assess HLA predisposition across two different ethnic populations. DESIGN AND SETTING: Patients were 126 men and 58 women referred to the Montpellier Sleep Disorders Center (Mtp) and 12 men and 8 women referred to the Fort-de-France Sleep Disorders Center (FdF) (Martinique, a French West Indy island) with symptoms of narcolepsy. PARTICIPANTS: Narcoleptics were included if they had both excessive daytime sleepiness and clear-cut cataplexy (for the group with cataplexy), a mean sleep latency of less than 8 minutes and at least two sleep onset REM periods. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Narcolepsy without clear-cut cataplexy was rare (12/172) in the Mtp population whereas it was as frequent as full-blown narcolepsy (10/10) in the FdF population. Comparison between narcoleptics with cataplexy from the Mtp and FdF populations revealed a younger age of onset, a trend towards more severe sleepiness and lower frequency of cataplexy in Martinicans. Comparison between narcoleptics without cataplexy from the Mtp and FdF population revealed a higher frequency of hypnagogic hallucinations and sleep paralysis and a trend towards more severe sleepiness in Martinicans. 4.2% of the Mtp and 15% of the FdF patients were negative for HLA DR2. However all of them were positive for HLA DQ1. Moreover, a tight association with HLA DRB1*1503 was observed in Martinicans in contrast with DRB1*1501 in the Mtp population. Association with HLA DQB1*0602 was observed in 99.4% of narcoleptics with cataplexy and in 89.5% of those without cataplexy. CONCLUSIONS: Narcolepsy is a heterogeneous clinical syndrome, the more so as ethnic origins are considered. A modulating effect of HLA and non-HLA genes on symptoms disease may explain these differences.

Adult↗
PubMed2006

Plasma levels of tumor necrosis factor alpha and soluble tumor necrosis factor receptors in patients with narcolepsy.

BACKGROUND: Narcolepsy is a disabling sleep disorder characterized by excessive daytime sleepiness, cataplexy, hypnagogic hallucinations, and sleep paralysis. Recent studies suggest that the immune system might play a pathogenic role pointing to a possible involvement of inflammatory cytokines. METHODS: We investigated a sample of 30 patients with narcolepsy in comparison with 120 sex- and age-matched and 101 sex-, body mass index (BMI)-, and age-matched randomly selected normal controls. In these groups, plasma concentrations of tumor necrosis factor alpha (TNF-alpha) and its soluble receptors p55 and p75 (soluble TNF receptor [sTNF-R] p55 and sTNF-R p75) were measured using commercial enzyme-linked immunosorbent assays. RESULTS: The narcoleptic patients showed a significantly higher BMI compared with controls of the same age. Soluble TNF-R p75 levels were consistently elevated in the narcoleptic patients compared with their sex- and age-matched (P = .001) as well as sex-, BMI-, and age-matched counterparts (P = .003). Female narcoleptic patients exhibited higher sTNF-R p55 levels compared with their sex- and age-matched controls (P = .01), but this difference disappeared when comparing patients with sex-, BMI-, and age-matched normal controls. Tumor necrosis factor alpha levels did not differ significantly between groups. CONCLUSION: Narcoleptic patients show increased plasma levels of sTNF-R p75, suggesting a functional alteration of the TNF-alpha cytokine system, further corroborating a possible pathogenic role of the immune system in this sleep disorder.

Body Mass Index↗
PubMed1994

Narcolepsy in children.

The clinical and polygraphic characteristics of narcolepsy in children were established on the analysis of 97 reported cases in children (including 12 personal cases). In idiopathic narcolepsies (77 cases) narcoleptic attacks occurred in 97% of the cases, cataplexy in 80.5%, hypnagogic hallucination in 39% and sleep paralysis in 29%; 13% of the children had the tetrad; dyssomnia was a prominent feature. Polygraphic data showed no significant differences between adults and children. In symptomatic narcolepsies (20 cases): cataplexy was the prominent feature occurring in 95% of the cases, 26% of the children had status cataplecticus; in these narcoleptic-cataplectic syndromes there was often an absence of polygraphic evidence of narcolepsy. Symptomatic narcolepsy should be suspected in cases where narcolepsy is detected in preteenage children, where cataplectic attacks are abnormally frequent, where there is an absence of polygraphic evidence of classical narcolepsy (although this criterion may not apply in the case of younger children) or where human leukocyte antigen typing for DR2 is negative. An association with a Niemann-Pick disease type C was found in 12 out of the 20 symptomatic cases, this association merits further study.

Catalepsy↗
PubMedDate not supplied

Genetic studies in narcolepsy, a disorder affecting REM sleep.

Narcolepsy is a disabling sleep disorder characterized by excessive daytime sleepiness and abnormal manifestations of rapid eye movement (REM) sleep including cataplexy, sleep paralysis, and hypnagogic hallucinations. It is known to be a complex disorder, with both genetic predisposition and environmental factors playing a role. In humans, susceptibility to narcolepsy is tightly associated with a specific HLA allele, DQB1*0602. In humans and canines, most cases are sporadic. In Doberman pinschers and Labrador retrievers, however, the disease is transmitted as an autosomal recessive gene canarc-1 with full penetrance. This gene is not linked with the dog leukocyte antigen complex, but is tightly linked with a marker with high homology to the human mu-switch immunoglobulin gene. We have isolated several genomic clones encompassing the canarc-1 marker and the variable heavy chain immunoglobulin region in canines. These have been partially sequenced and have been mapped onto specific dog chromosomes by fluorescence in situ hybridization (FISH). Our results indicate that the mu-switch-like marker is not part of the canine immunoglobulin machinery. We are continuing to extend the genomic contig using a newly developed canine BAC library and attempting to identify the corresponding human region of conserved synteny.

Animals↗
PubMed2007

[Sleep and movement disorders].

The three different states of being (wakefulness, NREM and REM sleep) are associated with profound neurophysiological and neurochemical changes in the brain. These changes explain the existence of movement disorders appearing only or preferentially during sleep, and the effects of sleep on movement disorders. Sleep-related movement disorders are of clinical relevance for multiple reasons: 1) high frequency (e.g. restless legs syndrome (RLS)); 2) diagnostic relevance (e.g. REM sleep behavior disorder (RBD) as first manifestation of Parkinson disorder); 3) diagnostic uncertainty (e.g. parasomnias vs nocturnal epilepsy); 4) association with injuries (e.g. RBD, sleepwalking), sleep disruption/daytime sleepiness (e.g. RLS), and psycho-social burden (e.g. enuresis); 5) requirement of specific treatments (e.g. nocturnal epilepsy, stridor, RBD). This article gives an overview on clinical manifestations, pathophysiology, work-up and treatment of sleep-related movement disorders (e.g. RLS, bruxism), parasomnias (e.g. sleepwalking, RBD), sleep-related epilepsies, and on sleep-associated manifestations of movement disorders (e.g. Parkinson disease, multiple system atrophy).

Adult↗
PubMed2002

Parasomnias decline during pregnancy.

OBJECTIVES: A survey of the effects of pregnancy on parasomnias. MATERIAL AND METHODS: In an area of a central hospital and the maternity care units in the nearby rural community, women were interviewed during and after their pregnancy with a series of five questionnaires to assess the frequency of their parasomnias. The first questionnaire covered the 3 months before becoming pregnant, the next three the trimesters of pregnancy and the last one the 3 months after delivery. Altogether 325 mothers filled all the five questionnaires and constitute the study group. RESULTS: The total number of parasomnias declined (P < 0.001) during pregnancy and even more among the primiparas than among the multiparas (difference until third trimester, P=0.02). Among various parasomnias reported, sleep talking and sleepwalking decreased from the prepregnant period to the second trimester (22.8 vs 12.6%, change P=0.003), and the reported sleep starts also diminished from the prepregnant time to the first trimester (78.5 vs 63.1%, P < 0.001), but these phenomena did not change further during the follow-up. Altogether 55.7% of the women reported having nightmares 3 months before the pregnancy, and 47.7, 49.5, 41.2 and 40.3% (change from the prepregnant period, P < 0.001), respectively, at first, second and third trimester and after the delivery. Reported hypnagogic hallucinations decreased from the prepregnant time to the first trimester (9.8 vs 6.5%, P=0.027), but returned thereafter to the previous level. During the prepregnant period, 25.8% of the women reported bruxism and only 19.9% during the first trimester (P=0.009). Though the prevalence of sleep paralysis decreased during the first trimester of pregnancy, it was the only parasomnia that increased during later pregnancy (from 5.7 to 13.3% in the second trimester, P < 0.013). CONCLUSIONS: The reported frequency of most parasomnias decreases during pregnancy and even more in primiparas than multiparas.

Adolescent↗