Management of Central Disorders of Hypersomnolence in Pregnancy and Lactation.

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Learn more: PMC Disclaimer | PMC Copyright Notice J Prim Care Community Health . 2026 May 29;17:21501319261456031. doi: 10.1177/21501319261456031 Management of Central Disorders of Hypersomnolence in Pregnancy and Lactation Zain Ul Abideen 1 , Bhanu Prakash Kolla 2, 3 , Matthew E Bernard 1 , Dominika A Jegen 1 , Joseph W Furst 1 , Meghna P Mansukhani 1, 3, ✉ Author information Article notes Copyright and License information 1 Department of Family Medicine, Mayo Clinic, Rochester, MN, USA 2 Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN, USA 3 Center for Sleep Medicine, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, MN, USA ✉ Meghna P. Mansukhani, MD, FAASM, Department of Family Medicine, Mayo Clinic, Rochester, MN, USA; Center for Sleep Medicine, Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, 200 First St SW, Rochester, MN 55905, USA. Email: mansukhani.meghna@mayo.edu Received 2026 Mar 12; Revised 2026 May 1; Accepted 2026 May 18; Collection date 2026 Jan-Dec. © The Author(s) 2026 This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/ ) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage ). PMC Copyright notice PMCID: PMC13221597  PMID: 42212348 This article has been corrected. See J Prim Care Community Health. 2026 Aug 23;17:21501319261481568 . Abstract Over 37% of pregnant women report excessive daytime sleepiness or hypersomnia during the first trimester, and commonly throughout the remaining trimesters of pregnancy and the postpartum period. The clinical presentation and symptoms of central disorders of hypersomnolence (CDH) such as narcolepsy, idiopathic hypersomnia, or excessive daytime sleepiness secondary to shift work or obstructive sleep apnea may be confounded by physiological changes in sleep architecture and hormonal fluctuations occurring during pregnancy. These overlapping features may cause delays in diagnosis and treatment, impacting quality of life, maternal functioning, and overall health. Management of CDH during pregnancy and lactation requires careful consideration of maternal benefits, potential side effects of medications and fetal and neonatal safety. Here, we present a case of idiopathic hypersomnia and detail management and outcomes during pregnancy and lactation. We briefly review the existing literature on prevalence, pathophysiological mechanisms, diagnostic challenges, objective findings, and risks posed by CDH in pregnancy and lactation. In this narrative review for primary care clinicians, we also summarize currently available evidence regarding the efficacy, teratogenic and other risks of pharmacologic agents used in the treatment of CDH in pregnancy and lactation. Lastly, we provide a clinical algorithm for management of CDH during pregnancy and lactation. Keywords: hypersomnia, hypersomnolence, sleepiness, narcolepsy, breastfeeding, gestation, medications, pharmacologic, treatment Introduction Excessive daytime sleepiness is frequently reported during pregnancy and the postpartum period and is often attributed to physiologic hormonal and sleep architecture changes. 1 , 2 However, in some individuals, hypersomnolence reflects an underlying central disorder of hypersomnolence (CDH), such as narcolepsy or idiopathic hypersomnia. Distinguishing pathologic hypersomnolence from expected gestational fatigue can be challenging, and untreated CDH may result in significant functional impairment and safety concerns. 3 Management of CDH during pregnancy and lactation is complex. 4 Evidence regarding the safety of wake-promoting medications is limited and largely derived from observational studies and pregnancy registries, requiring careful risk–benefit assessment and multidisciplinary collaboration. In this case-based narrative review, we present the longitudinal management of idiopathic hypersomnia (IH) before, during, and after pregnancy, and summarize current evidence to provide a practical framework for clinicians caring for pregnant and breastfeeding patients with CDH. Case Presentation A sixteen year-old female presented to primary care with weight gain, fatigue, restless sleep, frequent nightmares, snoring, and difficulty initiating and maintaining sleep. She was referred to Sleep Medicine. Her initial evaluation resulted in a diagnosis of generalized anxiety, and polysomnography (PSG) showed an apnea-hypopnea index of 0 per hour with an elevated periodic limb movement index of 6.6 per hour. She was referred to Psychiatry and commenced on gabapentin 400 mg nightly along with cognitive behavioral therapy for insomnia. Four years later, she returned with persistent daytime sleepiness. Her medications included fluvoxamine 100 mg, iron/folic acid, cyanocobalamin, and norethindrone-mestranol. To ensure accurate testing, psychotropic medications were tapered and discontinued before repeating actigraphy, PSG, and conducting a multiple sleep latency test (MSLT). Actigraphy and PSG were unremarkable. The MSLT demonstrated a mean sleep latency of 5.1 minutes with one sleep-onset rapid eye movement (REM) period across five naps, consistent with idiopathic hypersomnia. She was started on modafinil 200 mg daily and demonstrated sustained improvement on follow-up. During a follow-up visit five years later at the age of twenty-fiveyears, the patient indicated a desire to become pregnant. Prior to conception, the risks and benefits of continuing modafinil during pregnancy were thoroughly discussed. Given the patient’s family history of congenital malformations, she was referred to Maternal Fetal Medicine. She expressed concerns about her ability to function normally in daily life without the modafinil. Following collaborative decision making with the Maternal-Fetal Medicine and Sleep Medicine teams, and based on the patient’s preference, it was agreed that the continuation of modafinil with frequent follow-ups and perinatal monitoring would be implemented.This decision was guided by the understanding that the benefits of maintaining wakefulness and functioning significantly outweighed the potential teratogenic and maternal risks. She continued with routine follow-up in the sleep medicine clinic. During gestational weeks thirteen to sixteen, she reported nausea and fatigue, which was resolved without intervention. She consistently obtained approximately eight hours of sleep nightly and continued to tolerate modafinil with no new side effects. She reported preserved functioning and good daytime alertness, stable mood, and adherence to prenatal care with no obstetric complications. She had a normal vaginal delivery with infant Apgar scores of eight and nine at one and five minutes, respectively. A shared decision was made to continue modafinil in the postpartum period. She opted to breastfeed and at follow-up 9 months later, the patient reported continued daytime alertness, no medication side effects, and stable mood and her baby continued to show normal development. Discussion Background Sleep disturbances are common in pregnancy and the postpartum period. 5 Sleep disorders associated with pregnancy were recognized as a separate entity by the American Academy of Sleep Medicine in 2000 6 ; defined as the occurrence of insomnia or excessive daytime sleepiness during pregnancy. 1 Excessive daytime sleepiness or hypersomnia is an inability to stay alert and awake during a major part of the day, resulting in an irresistible need to sleep or unintentional lapses into sleep. Hypersomnia is a key symptom that results in impaired functioning in CDH, which are further classified into various subtypes as noted in Table 1 7 , 8 Notably narcolepsy type 1 refers to patients with narcolepsy and cataplexy, whereas narcolepsy type 2 refers to patients with narcolepsy without cataplexy. 8 Table 1. Classification of Central Disorders of Hypersomnolence 5 Central disorders of hypersomnolence 1. Narcolepsy type 1 2. Narcolepsy type 2 3. Idiopathic hypersomnia 4. Kleine-Levin syndrome 5. Hypersomnia due to a medical disorder 6. Hypersomnia due to a medication or substance 7. Hypersomnia associated with a psychiatric disorder 8. Insufficient sleep syndrome Open in a new tab Pregnancy introduces physiological sleep changes (sleep fragmentation, hormonal fluctuations, circadian shifts) and can potentially accentuate the symptoms of CDH. 9 Progesterone, estrogen, oxytocin, prolactin, and cortisol can all affect sleep patterns. Furthermore, these disorders can worsen in the context of sleep disruption occurring during the postpartum period and lactation. Management of CDH in pregnancy and lactation is similar in some respect to that in non-pregnant patients, particularly as it pertains to nonpharmacologic measures, as noted in a prior review of 744 studies (1991-2021). 9 However, it requires individualized decision making and a careful balance between maternal safety, fetal well-being, and medication-related risks. 10 The primary objective of this review is to summarize the current literature on the management of CDH in pregnancy and lactation. This review discusses the types of CDH, their prevalence and predictors, pathophysiology and implications, and diagnosis and therapy in pregnancy and lactation. This review helps inform current clinical practice and emphasizes areas for targeted research and the need for clinical guidelines to optimize patient care. Methods In this narrative review, we discuss the use of stimulant medications or other wake promoting agents prescribed for CDH in pregnancy and lactation. A comprehensive literature search was conducted in PubMed, Embase, an Scopus using different keyword strings and Boolean operators (AND, OR) to identify and retrieve relevant articles. The search string included sleep-related disorders using Medical Subject Headings (MeSH) terms, including “idiopathic hypersomnia”, “insufficient sleep syndrome”, “narcolepsy”, “Excessive Daytime Sleepiness”, and “disorders of excessive somnolence”. For medications, terms like “stimulants”, “wake promoting agents” were used to include modafinil, armodafinil, methylphenidate, amphetamine, dextroamphetamine, , solriamfetol, pitolisant, and oxybate. Further details regarding the search strategy are included in the Supplement . English language publications of adult subjects were included. We selected articles based on their relevance to this review, as stated by their title and abstract. Articles were chosen based on comprehensiveness and topic-related insight, ranging from systematic reviews, meta-analyses, and original studies to randomized controlled trials (RCTs) and large observational studies. Additionally, the reference lists of review articles were examined to look for additional relevant articles. Except for foundational references, articles published within the last 15 years (2010-until November 30, 2025) were selected. Prevalence and Predictors Sleep disturbances and changes in sleep patterns start early during the first trimester of pregnancy, with more significant changes evident around 11-12 weeks’ gestation. 11 - 13 During pregnancy, most women experience some degree of sleep disturbance and daytime fatigue, despite having a total sleep time often equal to, or exceeding that, in the pre-pregnancy period. High circulating hormone levels and physiological changes in pregnancy result in alteration of sleep architecture. When appropriate, initial treatment should focus on sleep-hygiene measures and behavioral therapies aimed at managing physical discomfort. In more severe cases, cognitive behavioral therapy for insomnia and/or short-term pharmacologic intervention may be necessary. 14 , 15 Sleep disruption associated with pregnancy may induce or exacerbate CDH. Predictors of worsening sleep patterns in pregnancy include increased nocturnal awakenings, iron deficiency, coexisting restless legs syndrome (RLS)/periodic limb movement disorder, anxiety, depression, and sedative medication exposure. 12 , 16 Diagnosis and Findings During Pregnancy It remains unclear to what extent physiological and pathologic sleep disruption in pregnancy may precipitate or worsen symptoms of CDH. 15 , 17 , 18 As pregnancy alters sleep architecture, diagnostic testing (PSG, MSLT) is generally not as reliable during pregnancy as in pre-pregnancy, and there is a general paucity of medical literature on this topic. 6 PSG studies of pregnant women demonstrate that the duration of REM sleep decreases from the first to second trimester. 19 Most significant changes in sleep continuity and architecture are seen in the third trimester, with numerous studies reporting an increase in wakefulness after sleep onset compared to the earlier trimesters. 11 , 20 - 22 During the final trimester, women have longer sleep duration but lower sleep efficiency due to increased wake time after sleep onset and longer sleep latency. 11 , 20 REM sleep and non-REM sleep stages N3 and 4 (deep or slow wave sleep) decrease, while stage N1 (light sleep) increases. 21 , 22 Studies including objective tests of daytime somnolence and results from MSLT in pregnancy are lacking. Pathophysiology and Pregnancy Interaction Sleep is disturbed in pregnancy and the postpartum period for many physiological reasons. 1 , 23 , 24 Sleep disorders can impact pregnancy and have been associated with several adverse outcomes including gestational hypertension, preeclampsia, impaired labor progression, preterm birth and growth restriction. 9 , 25 , 26 Estrogen and progesterone receptors are present in several brain regions involved in sleep and arousal regulation such as the preoptic area, suprachiasmatic nucleus, locus ceruleus, and other hypothalamic nuclei. 27 , 28 Estrogen and progesterone alter sleep architecture by modulating neural transmission through GABA receptor modulation in these areas related to sleep/wake regulation. 29 High levels of progesterone released from the placenta may have a soporific effect, contributing to feelings of sleepiness and fatigue. 3 , 24 Excessive daytime sleepiness (hypersomnia) is reported by many pregnant women and is often linked to poor nighttime sleep quality. 30 Causes of poor sleep include frequent awakenings due to OSA or PLMs. 31 Narcolepsy is thought to be due to a deficiency of hypocretin in the central nervous system. 32 Although several complex factors are at interplay, while IH involves impaired wake-promoting pathways, and possibly GABA-A receptor hypersensitivity. 33 While no definitive mechanisms have been identified for the development of hypersomnia during the postpartum period, it is hypothesized that insufficient sleep, hormonal changes, and sensitivity of neuronal receptors are key contributing factors. Maternal–Fetal Implications of Untreated CDH Sleep disturbances (including short or long sleep and poor sleep quality) in pregnancy are strongly associated with adverse maternal and neonatal outcomes [adjusted odds ratio (OR): 1.25-3.37], including increased risk of gestational diabetes mellitus, preterm birth, and other pregnancy complications. 34 Sleep disorders (e.g., insomnia, OSA, extremes of sleep duration) have been associated with increased systemic inflammation, a key mechanistic pathway implicated in gestational hypertension and preeclampsia. 35 Objective data in a metanalysis showed that maternal sleep disruption was associated with adverse fetal outcomes such as low birthweight and small for gestational age infants [adjusted ORs (95% CI); 1.4 (1.1,1.9)], and preterm birth [adjusted ORs (95% CI); 1.6 (1.2,2.2)], similar to that reported in multiple epidemiological studies. 36 , 37 Although existing evidence is limited, narcolepsy and IH have been associated with impaired glucose metabolism and anemia in pregnancy. 10 Nevertheless, overall pregnancy outcomes in treated individuals are broadly comparable to those in controls. 10 Pharmacotherapy in Pregnancy In this section, we review the main pharmacological agents used in the treatment of CDH, namely modafinil, armodafinil, methylphenidate, amphetamine/dextroamphetamine, solriamfetol, pitolisant, and oxybate formulations. Since some of the medications used to treat CDH are also used for the management of attention deficit hyperactivity disorder (ADHD), literature examining their safety in pregnancy when used for ADHD is discussed. These safety data can be extrapolated to the management of CDH during pregnancy with the caveat that the doses of the stimulant medications used for the treatment of CDH are sometimes higher than those used to treat ADHD. The literature on the effects of these medications in pregnancy and lactation is summarized in Table 2 . Table 2. Evidence Summarizing Effects of Stimulant Medications in Pregnancy and Lactation Medication Major malformation risk Growth effects Neurodevelopment Lactation Key evidence Modafinil No increased MCA 1 (%) Possible ↓BW 2 , ↓HC 3 (dose-dependent) Limited data Insufficient text ENTIS 2024, 36 Kaplan S. et al. Methylphenidate No overall ↑ malformations; slight signal for cardiac malformations No major effect No ↑ NDD 4 Very low transfer Huybrechts 2017, 41 Andrade 2018 43 Atomoxetine No ↑ MCA (OR 1.14; NS) no adverse perinatal growth outcomes reported across included registry studies Limited long-term data Insufficient evidence Giacomo 2024 42 Amphetamines/Dextroamphetamines No ↑ malformations Slight risk ↓BW/preterm birth; inconsistently seen No ↑ NDD 3 Compatible Suarez 2024, 38 Ornoy 2021 46 Solriamfetol Insufficient human pregnancy outcome data Insufficient data Lack of neurodevelopmental data Present in breast milk (RID 5 ∼5.5%); infant monitoring advised Drugs and Lactation Database (LactMed®) 2006 83 Pitolisant Insufficient human pregnancy outcome data Insufficient data Lack of neurodevelopmental data Low–moderate milk transfer reported; limited outcome data Drugs and Lactation Database (LactMed®) 84 Sodium oxybate/mixed oxybates Animal studies show adverse outcomes at high doses Insufficient data Insufficient data Excreted in human milk; caution advised E.C. Barker et al. 85 Open in a new tab 1 (MCA) Major congenital anomalies. 2 (BW) Birthweight. 3 (HC) Head circumference. 4 (NDD) Neurodevelopmental disorders. 5 (RID) Relative infant dose. Modafinil and Armodafinil Modafinil is approved by the United States (US) Food and Drug Administration (FDA) for the treatment of excessive daytime sleepiness relating to shift work disorder, OSA, Parkinson’s disease, narcolepsy, and is used off label in the treatment of IH. 4 Modafinil has been shown to significantly improve self-reported sleepiness on the Epworth Sleepiness Scale by 5.08points compared to placebo (95% CI: 3.01-7.16). 38 Observational cohort data and pregnancy registry reports provide the primary source of human evidence for the use of modafinil in pregnancy; RCTs are lacking in this area and overall data are limited. 38 , 39 , 47 In 2021, Kaplan et al reported data from a US voluntary pregnancy registry that identified a higher-than-expected rate of major congenital malformations among modafinil-exposed pregnancies. Following this, the European Medicines Agency and other regulatory bodies issued precautionary statements advising against the regular use of modafinil during pregnancy; several of these advisories remain publicly accessible today. 38 Voluntary registries have inherent biases; population-based controlled studies demonstrate no elevated risk (risk ratio of 1.06 [95% CI: 0.35-3.25]) for major congenital malformations among infants exposed to modafinil during the first trimester compared to the background population risk. 40 A recent case series conducted by European Network of Teratology Information Services (ENTIS) concluded that in utero exposure to modafinil was not associated with an increased risk of major congenital anomalies, but there was a tendency toward lower birth weight and reduced neonatal head circumference. Each 100 mg increase in modafinil dosage was associated with a decrease in standard deviation scores (SDS) of -0.28 SDS (95% CI: -0.45 to -0.10) of birth weight and of -0.28 SDS (95% CI: -0.56 to 0.01) of head circumference. The authors concluded that high doses (>400 mg/day) may affect fetal growth, necessitating growth surveillance. 39 There is no current data on the use of armodafinil for CDH in pregnancy. Given the potential association of modafinil with adverse pregnancy outcomes, childbearing potential should be considered before prescribing these medications. 48 Their use should be considered during pregnancy only in exceptional and complex cases of severe hypersomnia in which maternal benefit clearly outweighs potential fetal risks. This requires informed decision-making with patients, continuous monitoring, and close multidisciplinary collaboration among primary care, sleep medicine, psychiatry, obstetrics, and maternal-fetal medicine specialists. Data regarding the use of these medications in breastfeeding mothers is lacking. Methylphenidate Preparations Methylphenidate is FDA approved for the treatment of narcolepsy. Data from National Toxicological Program Centre for the Evaluation of Risks to Human Reproduction (CERHR) and large population-based studies show no increased risk of major congenital malformations associated with methylphenidate in mothers receiving this medication for the treatment of ADHD. 42 , 49 , 50 However, these studies suggested a small, dose-independent increase in cardiac malformations with first-trimester exposure to methylphenidate [OR 1.59; 95% CI 1.02-2.49)], corresponding to a modest absolute risk increase. 50 According to data from Huybrechts et al, methylphenidate use during pregnancy was not significantly associated with major overall malformation risk (relative risk [RR] 1.11; 95% CI: 0.91–1.35; p>0.05) or cardiovascular malformation risk (RR 1.28; 95% CI: 0.94-1.74; p>0.05). 51 A more recent systematic review and meta-analyses of over 16,000,000 pregnant women did not reveal an increase in congenital anomalies (OR, 1.14; 95% CI, 0.83-1.55; P = .4) or miscarriages (OR, 1.15; 95% CI, 0.82-1.62) in mothers receiving treatment with methylphenidate or a combination of methylphenidate and atomoxetine. 52 More recent data indicate no meaningful increase in autism spectrum disorder [hazard ratio (HR) 1.06; 95% CI: 0.62-1.81] or global neurodevelopmental disorders (HR 1.15; 95% CI: 0.97-1.36) following in utero exposure to methylphenidate, after accounting for confounding by maternal attention deficit hyperactivity disorder and illness severity. 49 , 51 During lactation, methylphenidate is excreted in breast milk at low concentration, with minimal reported adverse events in nursing infants. 53 When clinically indicated, it is generally considered compatible and safe with breastfeeding. Currently available cohort data do not demonstrate a significant increase in major congenital malformations, though individualized risk–benefit assessment remains essential when prescribing this medication in pregnancy and in the postpartum period. 54 Amphetamine/Dextroamphetamine The immediate release preparation of amphetamine/dextroamphetamine is FDA approved for the treatment of narcolepsy. Evidence from multiple cohorts of women receiving amphetamine/dextroamphetamine for ADHD indicates that there is no associated risk of cardiac or major malformations with amphetamine/dextroamphetamine after adjustment for potential confounders. 55 , 56 There is a slight increase in the associated risk of premature birth/low birth weight in infants in some analyses, although these findings have not been consistently observed across studies. 49 Neurodevelopmental follow-up data suggests that there is no increase in atrial septal defect (HR 0.80; 95% CI: 0.56 - 1.140), ADHD (HR 1.07; 95% CI: 0.89-1.28; p>0.05), or neurodevelopmental disorders (HR 0.91; 95% CI: 0.81-1.28) in children exposed to amphetamines/dextroamphetamine in utero. 49 , 51 , 57 According to Huybrechts et al amphetamine was not associated with an increased risk of physical malformations (RR 1.05; 95% CI: 0.93–1.19; p> 0.05) or cardiovascular malformations (RR 0.96; 95% CI: 0.78–1.19; p>0.05). 54 Further studies are needed to determine whether it is safe to continue these medications in pregnancy, and, if not, when these should be optimally discontinued. 58 Current evidence suggests that amphetamine/dextroamphetamine may be considered when maternal functional impairment is significant and after individualized risk–benefit assessment. 54 , 58 - 60 Solriamfetol Solriamfetol is a novel pharmacologic agent which exerts its effect by inhibiting the reuptake of dopamine and norepinephrine, thereby increasing dopamine availability in the synaptic cleft. It has shown efficacy with a reasonable safety profile in multiple phenotypes of hypersomnia (OSA, narcolepsy types 1 and 2, Parkinson’s disease), as compared to placebo. 56 - 69 It is currently FDA approved for the treatment of narcolepsy and excessive daytime sleepiness secondary to OSA. Unlike conventional stimulants such as dextroamphetamine and methylphenidate, solriamfetol has a lower potential for cardiovascular adverse events and minimal withdrawal symptoms. 70 A recent analysis, by He et al, of the FDA Adverse Event Reporting System identified spontaneous pregnancy loss associated with solriamfetol use. 71 Similarly, a retrospective analysis reported possible associations of spontaneous abortion events with pitolisant, sodium oxybate, solriamfetol, and modafinil in the management of narcolepsy, warranting further investigations and additional safety assessment of these medications in the pre-pregnancy and early pregnancy periods. 72 Despite evidence supporting the efficacy of solriamfetol for CDH, real-world data is lacking on the efficacy and safety profile of solriamfetol for its use during pregnancy and lactation. Long-term interventional studies are needed in these patient populations. Pitolisant Pitolisant is a potent and highly selective histamine 3 receptor antagonist/inverse agonist that is FDA approved for the treatment of excessive daytime sleepiness or cataplexy in adult patients with narcolepsy. 70 In open label and placebo controlled trials, pitolisant resulted in improvements in sleepiness, sleep inertia, and a multitude of functional outcomes in patients with narcolepsy, with minimal safety concerns. 58 , 73 Its safety and efficacy profile in pregnancy and lactation is not well established. A prospective, observational cohort study designed to evaluate the association between pitolisant exposure during pregnancy and subsequent maternal, fetal, and infant outcomes is currently ongoing and expected to be completed in 2030. 74 Oxybates Sodium oxybate is FDA approved for the treatment of narcolepsy, and mixed-salt oxybate for narcolepsy and IH, respectively. Although exact pharmacologic mechanisms of action are currently unclear, gamma hydroxybutyrate (GHB) or oxybate, is hypothesized to act through the activation of gamma-aminobutyric acid type B (GABA B ) receptors which block the actions of noradrenergic and dopaminergic neurons as well as the thalamocortical neurons. 67 GHB increases the percentages of stages N2 and N3 sleep, decreases stage N1 and REM sleep and reduces the number of nighttime awakenings in adults. 75 It has been shown to significantly reduce daytime sleepiness in patients with narcolepsy and IH. 76 , 77 Prospective real-world studies are required in order to establish the association between oxybates and maternal and fetal outcomes in patients with CDH during pregnancy. Similarly, there is currently insufficient evidence regarding the risk to breast-fed infants and the effect on milk production in breastfeeding mothers. In a survey of sleep specialists, 77% advised stopping sodium oxybate for sleepiness,19% suggested reducing the dose, and 4% recommended continuing the medication with the dose unchanged. 78 A case report of a 27-year-old female using sodium oxybate during lactation indicated that the infant demonstrated appropriate growth and development for the first 6 months of life without any apparent adverse effects of the medication. 77 Sodium oxybate has insufficient human pregnancy safety data supporting its use. Its use in pregnancy should therefore be reserved for highly exceptional circumstances in which the severity of symptoms poses an immediate safety risk to the mother and fetus, and no alternative pharmacotherapy is tolerated. 72 Other Medications Antidepressants have demonstrated efficacy in the management of cataplexy, a hallmark symptom of narcolepsy type 1, as well as other symptoms related to the dysregulation of REM sleep. Antidepressants, including selective serotonin reuptake inhibitors and serotonin norepinephrine reuptake inhibitors, suppress REM sleep and reduce the frequency of cataplexy episodes by increasing noradrenergic and serotonergic signaling, with minimal effects on hypersomnia. 79 Among them, venlafaxine, fluoxetine and duloxetine are the most commonly used agents for cataplexy with few reported adverse events. However, scientific data from clinical trials are lacking. 80 - 82 For many years tricyclic antidepressants such as protriptyline and clomipramine were used to treat cataplexy but have fallen out of favor due to their potential anticholinergic side effects. 83 While a detailed discussion of these pharmacological agents is beyond the scope of this review, selective serotonin reuptake inhibitors have been demonstrated to be associated with major congenital malformations, preterm birth, and other complications, although absolute risk increases remain small for most outcomes. 43 , 84 , 85 Non-Pharmacologic Management Optimization of sleep hygiene, including maintaining consistent sleep wake schedules, ensuring sufficient nocturnal sleep opportunity, avoidance of late-day caffeine intake, maintaining physical activity, and reduction of environmental sleep disruption are essential, particularly as sleep fragmentation increases across gestation. Structured sleep scheduling, complemented with planned daytime naps and bright light therapy, can help mitigate hypersomnia and improve functional safety during pregnancy. Screening for iron deficiency is critical, as low iron stores are common in pregnancy and contribute to RLS, PLMs, sleep disruption, and worsened hypersomnia. Iron repletion has been shown to improve sleep quality and daytime alertness in patients with other sleep disorders coexisting with RLS. 14 , 44 , 45 A proposed algorithm for the management of CDH in pregnancy and lactation is outlined in Figure 1 . Of note, pharmacotherapy is still required in most cases of CDH. 14 , 86 Figure 1. Open in a new tab Management algorithm for central disorders of hypersomnolence in pregnancy and lactation Comorbid Sleep Disorders Narcolepsy and IH are found to be associated with substantial psychiatric and other sleep comorbidities which contribute to hypersomnia requiring ongoing monitoring. 7 , 87 - 89 Treating comorbid sleep disorders can reduce sleep fragmentation and improve daytime alertness in patients with CDH. 90 RLS, a common condition in pregnancy, may negatively affect maternal wellbeing by contributing to stress and sleep disruption. 90 OSA remains a significant contributor to hypersomnia in the general population and can worsen in severity during pregnancy; it can exacerbate excessive daytime sleepiness in CDH if untreated or suboptimally treated. 86 Thus, all pregnant women should be screened and treated for sleep disturbances and comorbid sleep disorders, given the significant impact of inadequate sleep and sleep disorders on overall pregnancy, fetal, and postpartum outcomes. 91 Implications for Primary Care Clinicians Central disorders of hypersomnolence in pregnancy require individualized, function-focused management. Primary care clinicians play a central role in early recognition, risk stratification, medication counseling, and coordination of multidisciplinary care. • Differentiate physiological fatigue from pathological hypersomnolence. Persistent excessive daytime sleepiness that impairs driving, daily functioning, or infant care, particularly in patients with a prior diagnosis of narcolepsy or idiopathic hypersomnia, warrants further investigation. • Screen for, and address, reversible contributors. Evaluate patient iron deficiency status, mood disorders, medication side effects, restless legs syndrome, and obstructive sleep apnea before attributing worsening symptoms solely to pregnancy. • Prioritize non-pharmacologic strategies. Reinforce structured sleep schedules, planned daytime naps, optimization of nocturnal sleep opportunity, and management of comorbid sleep disorders. • Engage in shared decision-making when considering pharmacotherapy. Discuss known and unknown fetal risks, maternal functional necessity, and trimester-specific considerations. • Use the lowest effective medication dose and monitor closely. Coordinate with obstetrics and maternal–fetal medicine teams when continuing wake-promoting agents. Monitor maternal blood pressure, weight, mood, and sleep quality; consider fetal growth surveillance. • Provide safety counseling. Discuss driving precautions, occupational risk mitigation, and safe infant care strategies, particularly during the postpartum period. When to Refer Referral to sleep medicine is indicated for diagnostic uncertainty, worsening hypersomnolence despite optimized sleep hygiene, consideration of medication adjustments, or suspected narcolepsy with cataplexy. Collaboration with maternal–fetal medicine is recommended when continuing stimulant or wake-promoting medications during pregnancy, when high doses are required, or when fetal growth concerns arise. Early multidisciplinary coordination supports maternal functioning while safeguarding fetal outcomes. Conclusion CDH can persist or worsen during pregnancy and significantly impair maternal functioning. Nonpharmacologic strategies and behavioral recommendations remain first-line in pregnancy; however, pharmacologic treatment may be necessary for pregnant patients with severe, functionally impairing hypersomnia and are generally required for the treatment of most CDH. It should be noted that current evidence for CDH pharmacotherapy in pregnancy is mainly derived from retrospective studies, registries, and databases, with no prospective randomized controlled trials. High quality longitudinal studies are needed to explore pharmacotherapeutic options, particularly in head-to-head trials of efficacy and incorporating objective measures of sleepiness. When required, stimulant therapy should be individualized, dose-minimized, and preferably avoided during the first trimester in pregnancy due to fetal organogenesis. Methylphenidate and amphetamine derivatives may be considered after careful risk-benefit assessment and close obstetric monitoring, whereas modafinil should be reserved for exceptional cases. Multidisciplinary collaboration among primary care, sleep medicine, psychiatry, obstetric and maternal-fetal medicine specialists, and shared decision-making with the patient, are essential to optimize maternal alertness and safeguard fetal outcomes when prescribing these therapies in pregnancy and during the postpartum period. Supplemental Material Supplemental Material - Management of Central Disorders of Hypersomnolence in Pregnancy and Lactation sj-pdf-1-jpc-10.1177_21501319261456031.pdf (168.9KB, pdf) Supplemental Material for Management of Central Disorders of Hypersomnolence in Pregnancy and Lactation by Zain Abideen, Bhanu Prakash Kolla, Matthew E. Bernard, Dominka A. Jegen, Joseph W. Furst and Meghna P. Mansukhani in Journal of Primary Care & Community Health. Acknowledgements The authors received no writing, editing, or submission assistance for this manuscript and there is nothing to acknowledge. The manuscript has been written, revised, and submitted solely by the authors. Funding: The authors received no financial support for the research, authorship, and/or publication of this article. The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. 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