Polysomnographic and Clinical Characteristics of Narcolepsy in Saudi Arabia: A 12-Year Retrospective Study

Summary

Objective:

To evaluate the clinical features, polysomnographic findings, and therapeutic outcomes of narcolepsy type 1 and type 2 patients in Kingdom of Saudi Arabia (KSA). Narcolepsy is a neurological condition marked by excessive daytime sleepiness (EDS) and associated symptoms, including cataplexy and disrupted nighttime sleep. Data on narcolepsy in KSA are still limited.

Methods:

Forty-three patients diagnosed with narcolepsy from 2012 to 2024 were included in this retrospective study. Diagnosis followed the International Classification of Sleep Disorders criteria and incorporated clinical features, the epworth sleepiness scale (ESS), overnight polysomnography (PSG), and multiple sleep latency testing (MSLT). Data on demographics, clinical symptoms, PSG parameters, and treatment were analyzed. Posttreatment ESS scores were collected via an electronic survey.

Results:

All patients reported EDS, and 53.5% had cataplexy. Time of diagnosis mean age was 28.9 ± 14.4 years, with a diagnostic delay of 5.3 ± 3.0 years. Patients with narcolepsy type (NT)1 had significantly higher baseline ESS scores (19.6 versus (vs.) 16.9, p = 0.031) and shorter mean sleep latency (2.1 vs. 4.3 minutes, p = 0.008). Treatment, predominantly with modafinil (69%), significantly reduced ESS scores from 18.4 ± 4.2 to 9.2 ± 2.4 (p < 0.001).

Conclusion:

Compared with NT2, NT1 is slightly more common and is characterized by more severe sleepiness and shorter sleep latency time. The diagnostic delay remains substantial, but treatment is effective in reducing EDS.

Introduction

Narcolepsy is a chronic, disabling neurological sleep disorder marked by impaired sleep–wake cycle regulation, leading to excessive daytime sleepiness (EDS) with a range of auxiliary symptoms, including cataplexy (transient episodes of involuntary muscle atony), disturbed nighttime sleep, sleep paralysis and sleep-related hallucinations [1,2,3]. Narcolepsy is classified into 2 subtypes. Narcolepsy type 1 (NT1) is characterized by the presence of cataplexy and/or reduced cerebrospinal fluid (CSF) hypocretin-1 level (≤110 pg/mL or mean value less than one-third established by standardized assays). In contrast, NT2 is marked by the absence of cataplexy and generally present with normal level of CSF hypocretin-1 [1,2,3].

The estimated worldwide narcolepsy prevalence ranges from 25 to 67 per 100,000 people, but rates vary across populations [2]. In Asia, prevalence estimates remain heterogeneous, with higher rates reported in Japan and lower rates observed in other East Asian countries [4,5,6]. Recent epidemiologic data indicate a prevalence of approximately 37.5 per 100,000 individuals in Japan, whereas studies from South Korea and Taiwan report lower prevalence estimates ranging between 8.4 to 9.98 per 100,000 individuals [4,5,6]. These variations likely reflect differences in population demographics, genetic susceptibility, study methodology, healthcare-system factors, and diagnostic awareness. In Kingdom of Saudi Arabia (KSA), a comprehensive 2-phase door-to-door survey conducted in the Eastern Province screened more than 23,000 Saudi nationals and reported a prevalence of narcolepsy of approximately 0.04 per 1000 capita [7]. Despite its relatively low prevalence, both subtypes of the condition have a profound impact on quality of life, daily functioning, and safety, contributing to occupational difficulties, academic underachievement, and an increased risk of accidents [8].

The NT1 is most commonly attributed to the selective degeneration of hypocretin-producing neurons, a process thought to be mediated by autoimmune mechanisms, whereas the pathophysiology of NT2 remains less defined [2]. Notably, a link has been established between the development of NT1 and exposure to influenza A (H1N1) infection or vaccination, suggesting the presence of an autoimmune trigger in genetically susceptible individuals [9].

Diagnosis relies on a combination of clinical evaluation, epworth sleepiness scale (ESS) scoring, overnight polysomnography (PSG), and a multiple sleep latency test (MSLT) [10]. Narcolepsy age of onset varies widely; however, symptoms typically manifest within the first 2 decades of life and exhibit a bimodal distribution, with peaks at approximately 15 and 35 years of age [11]. However, owing to low disease awareness and overlapping symptoms with other disorders, diagnostic delays frequently exceed 5–15 years, increasing patient morbidity [12,13].

In KSA and the broader Middle East, research on narcolepsy is scarce, with studies on the differences in clinical presentations or PSG findings of narcolepsy in local populations compared with western populations being limited. Cultural perceptions, health care access, and referral patterns may influence narcolepsy identification and diagnosis in this region.

This study sought to assess and compare the clinical features, polysomnographic findings, and treatment outcomes of patients with different types of narcolepsy in a sleep center in KSA. Findings from this work may help bridge the current knowledge gap and improve diagnosis and management strategies for narcolepsy in the region.

Methods

This retrospective study was carried out at the Sleep Medicine and Research Center, King Abdulaziz University Hospital, Jeddah, KSA. Prior to study initiation, ethical approval was attained from King Abdulaziz University Ethical Review Committee. All patients who were diagnosed and managed for narcolepsy at the center between January 2012 and December 2024 were included.

Patients fulfilling narcolepsy diagnostic criteria as defined by the International Classification of Sleep Disorders, 3rd edition (ICSD-3), were included in the study [10]. The diagnosis was based on the following: EDS presence for at least 3 months, supported by either MSLT with a sleep latency mean ≤8 minutes with ≥2 sleep-onset rapid eye movement (REM) periods (SOREMPs) or ≥1 SOREMP and PSG evidence of REM sleep onset occurring within 15 minutes during overnight monitoring [10]. To mitigate the influence of chronic sleep insufficiency, we incorporated a sleep diary with a duration of 1 week as well as actigraphy prior to PSG for every case. This strengthens the validity of our findings by ensuring that the observed sleep disturbances are not confounded by habitual sleep deprivation.

Patients were further classified into NT1 (with cataplexy) or NT2 (without cataplexy) based on the history of cataplexy. Patients with secondary narcolepsy due to neurological or other medical disorders were excluded. Additionally, patients with missing essential diagnostic or outcome data, including incomplete PSG or MSLT results, missing ESS scores, or insufficient clinical documentation to reliably classify narcolepsy subtype, were excluded from the analysis.

Patient data were retrieved from the hospital's electronic medical records. The first registered case in the center was in 2012; therefore, records from 2012 to 2024 were reviewed. The extracted variables involved demographic information (age, sex, body mass index [BMI], and time interval from symptom onset to diagnosis), clinical presentation (EDS, cataplexy, sleep paralysis, hypnagogic and hypnopompic hallucinations, restless legs syndrome [RLS], and comorbid obstructive sleep apnea [OSA]) and treatment history.

All patients underwent an overnight Type 1 diagnostic PSG (SOMNO Medics Plus; SOMNO Medics, Randersacker, Germany) followed by an MSLT as per American Academy of Sleep Medicine (AASM) guidelines [14,15]. The PSG recordings involved electroencephalography, electrooculography, electromyography, electrocardiography, nasal pressure, nasal and oral airflow, chest and abdominal respiratory effort, pulse oximetry, tracheal microphone for snoring, and sensors for body position monitoring. Recorded parameters encompassed sleep latency, sleep efficiency (%), total sleep time, the apnea–hypopnea index (AHI), wakefulness after sleep onset (WASO), arousal index (AI), and the periodic limb movement (PLM) index. Respiratory events and PLM were scored manually as per AASM definitions [14,15]. The MSLT was performed the morning after PSG according to AASM guidelines consisting of 5 nap opportunities spaced at 2-hour intervals [16]. During each nap, patients lay quietly in a dark, quiet environment and attempted to fall asleep while the sensors measured sleep onset and stages. Each nap was concluded either 15 minutes from the onset of sleep or at 20 minutes in case the patient did not fall asleep, with the next nap commencing 2 hours later. Daytime sleep propensity was objectively measured by calculating mean sleep latency and the number of SOREMPs.

The ESS scores were recorded at baseline (the time of diagnosis) from the patient's history. Medication regimens initiated for narcolepsy management such as modafinil, methylphenidate, and combination therapy were documented. In early 2025, all patients were contacted and invited to complete an electronic survey to obtain posttreatment ESS scores [17]. Patients were initially invited to complete the ESS via an electronic survey; those who did not respond electronically were subsequently contacted by phone, and ESS responses were obtained verbally and documented by the research team. This approach ensured complete post-treatment ESS data for all patients included in the baseline analysis.

Statistical analysis

The SPSS version 23 was used for data analysis. Descriptive statistics were reported as mean ± standard deviation (SD) for continuous variables and frequency distributions with percentages for categorical variables. the Shapiro–Wilk test was used to assess data normality. Nonparametric statistical tests were applied as the data were not normally distributed. Comparisons of continuous variables between 2 independent groups for example, male versus (vs.) female, narcolepsy with vs. without cataplexy were assessed using The Mann–Whitney U test. Paired measures over time such as ESS before vs. after treatment were compared using the Wilcoxon signed-rank test. Statistical significance was defined as a 2-tailed p-value < 0.05.

Results

The analysis included a total of 43 patients with narcolepsy, comprising 26 (59.5%) men and 17 (40.5%). women Patients had a mean age of 28.9 ± 14.4 years at time of diagnosis, with a mean BMI of 27.7 ± 6.7 kg/m². Mean onset of symptoms to diagnosis time was 5.3 ± 3.0 years ranging from 1 to 12 years. Twenty three patients were classified as NT1 (53.5%), whereas 20 patients were classified as NT2 (46.5%).

In terms of clinical presentation, all patients (100%) reported EDS. Twenty-three patients (53.5%) presented with cataplexy, while 16 (37.2%) patients experienced sleep paralysis. Other accompanying symptoms were less frequent, with hypnagogic hallucinations reported in 5 (11.6%) patients and hypnopompic hallucinations in 6 (14%) patients shown in Fig. 1.

Fig. 1.

Presence of various sleep disorders and symptoms among the patients. EDS: excessive daytime sleepiness, RLS: restless leg syndrome, OSA: obstructive sleep apnea.

The PSG findings revealed a mean sleep latency of 13.5 ± 22.4 minutes, sleep efficiency of 79.8% ± 13.4, and mean AHI of 2.7 ± 3.4 events/hour. The mean AI was 15.7 ± 11.5 events/hour, and the mean WASO was 63.2 ± 51.9 minutes. The mean PLM index was 5.6 ± 10.1. On the MSLT, all patients demonstrated short sleep latencies, with a mean of 3.0 ± 2.5 minutes (Table 1).

Table 1.

Overnight polysomnography and MSLT findings.

Variables	Mean	SD
Epworth sleepiness scale	18.4	4.2
Sleep latency (min)	13.5	22.4
Sleep efficacy (%)	79.8	13.4
Apnea hypopnea index	2.7	3.4
Arousal index	15.7	11.5
Wake after sleep onset (min)	63.2	51.9
Multiple sleep latency time (min)	3.0	2.5
Periodic leg movements index (%)	5.6	10.1
Posttreatment ESS	9.2	2.4

MLST: multiple sleep latency test, SD: standard deviation, ESS: epworth sleepiness scale, MIN: minutes.

When the PSG and MSLT parameters were compared between men and women, the only significant difference was in the AHI, which was greater in men (3.8 events/hour) than in women (1.12 events/hour, p = 0.009). Other sleep parameters did not show any statically significant sex-based differences (Table 2). Comparisons between patients with NT1 and NT2 revealed that those with NT1 had significantly higher baseline ESS scores (p = 0.031) and shorter mean sleep latencies (p = 0.008) than those with NT2 did (Table 2).

Table 2.

Overnight polysomnography and MSLT scores in relation to sex.

	Sex			Narcolepsy type (NT)
Variables	Male	Female	P value	NT1	NT2	P-value
Baseline Epworth sleepiness scale	17.8 (4.1)	19.5 (4.1)	0.089	19.8 (3.0)	16.8 (4.8)	0.031 *
Sleep latency (min)	12.4 (20.7)	15.2 (25.2)	0.87	7.3 (9.6)	21.0 (30.3)	0.142
Sleep efficacy (%)	78.2 (15.6)	82.2 (9.2)	0.362	79.8 (9.7)	79.8 (17.2)	0.336
Apnea hypopnea index	3.8 (4.1)	1.12 (1.2)	0.004 *	3.5 (4.2)	1.8 (1.9)	0.142
Arousal index	16.4 (12.7)	14.7 (9.7)	0.758	13.9 (6.4)	17.8 (15.5)	0.889
Wake after sleep onset (min)	57.6 (52.8)	71.5 (51.1)	0.343	76.4 (56.5)	47.3 (42.0)	0.143
Multiple sleep latency time (min)	2.8 (2.7)	3.3 (2.4)	0.434	2.0 (1.6)	4.3 (2.9)	0.008 *
Periodic leg movements index (%)	3.1 (3.3)	9.3 (15.1)	0.321	7.3 (12.6)	3.5 (6.1)	0.089
Post treatment ESS	9.0 (2.4)	9.5 (2.5)	0.603	9.7 (12.5)	8.6 (2.6)	0.123

MSLT: multiple sleep latency test, ESS: Epworth sleepiness scale, MIN: minutes

^*statistically significant at the 0.05 level.

Among the medications prescribed, modafinil was prescribed to 69%, 16.7% were on methylphenidate, and 14.3% were on modafinil and fluoxetine. The mean ESS score at baseline was 18.4 ± 4.2, which significantly decreased to 9.2 ± 2.4 following treatment (p < 0.001).

Discussion

This retrospective study evaluated 43 patients who were diagnosed and managed for narcolepsy over a 12-year period at an academic center in the western region of KSA. The EDS was reported by all patients. The NT1 was diagnosed in 53.5% of the study sample, while 46.5% had NT2. The mean age at time of diagnosis was 28.9 ± 14.4 years, with an average diagnostic delay of 5.3 ± 3.0 years. The PSG evaluation revealed an elevated AI and WASO, indicating disrupted sleep continuity. Notably, compared with NT2 patients, patients with NT1 had significantly greater baseline ESS scores and shorter mean sleep latencies. Treatment, primarily with modafinil, was associated with a marked reduction in ESS scores.

In our study, NT1 accounted for 53.5% of the cases, while 46.5% had NT2. This distribution closely aligns with several clinical cohorts in which NT1 modestly predominated [18,19,20]. A similar local study from the central region reported 47 patients with narcolepsy (72% with NT1) whose clinical features were largely consistent with those in the Western literature [18]. Another recent nationwide survey of 299 Korea Narcolepsy Association members examined the clinical features, comorbid conditions, time to diagnosis, and patients’ quality of life. The study reported that 61.5% of patients had NT1, while 38.5% had NT2, with NT1 patients reporting more severe symptoms [19]. Similarly, a prospective 5-year follow-up study at Chang Gung Memorial Hospital in Taiwan assessed the long-term outcomes of 157 patients with narcolepsy. The study revealed an NT1 prevalence of 71% vs. 29% for NT2, reflecting the predominance of NT1 in specialized clinical settings [20]. In contrast, a large cohort study by Jiang et al. [21] utilized the Lehigh Valley Health Network (LVHN) in the United States of America involving 304 patients exhibited the opposite pattern, with NT2 comprising 82.9% of the cases and NT1 comprising only 17.1%. One plausible explanation for the higher NT1 proportions in several cohorts is that compared with NT2, NT1 tends to be more symptomatic and easier to recognize. This because of the presence of cataplexy and higher ESS, which typically prompt earlier referrals, leading to a higher prevalence and shorter diagnostic delay [1,2,3]. Additionally, the absence of cataplexy and the lower test–retest reliability of the MSLT in NT2 may contribute to under recognition, delayed, and unstable classification of this type [22]. These dynamics likely influence our observed distribution and should be considered when comparing subtype frequencies across settings and regions.

The EDS in patients with narcolepsy should be interpreted within the broader pathophysiological framework of this disorder, characterized by instability of sleep–wake regulation as well as fragmented nocturnal sleep resulting from the frequent arousals seen in these patients. In this context, our study revealed that patients with NT1 exhibited significantly higher baseline ESS (19.6 vs. 16.9, p = 0.031) and shorter mean sleep latencies on the MSLT (2.1 vs. 4.3 minutes, p = 0.008) compared to NT2. This reflects more severe EDS and a greater propensity to fall asleep during daytime naps that is more symptomatic than NT2. These observations are consistent with prior literatures highlighting the clinical distinctions between NT1 and NT2 [18,19,20,21,22,23,24]. Kim et al. [19] and Jiang et al. [21] reported significantly higher ESS scores observed in NT1 patients compared to NT2. Although Bahammam et al. [18] also reported higher ESS scores and shorter sleep latencies in NT1 patients than in NT2 patients, these differences did not reach statistical significance level. Moreover, Ruoff et al. [22] demonstrated that patients with NT1 had lower mean sleep latency (3.4 ± 0.4) in MSLT with more reproducibility and stability in 78% compared to NT2 (6.6 ± 0.5, 18%), suggesting that patients with NT1 have more severe, consistent and objective evidence of sleepiness. Additionally, Um et al. [23] reported that compared with NT2 patients, NT1 patients had significantly shorter sleep latencies on the MSLT, further supporting the notion of greater daytime sleep propensity in NT1 patients. Collectively, these findings highlight clear differences between NT1 and NT2, underscoring the importance of accurate subtype identification. NT1's pronounced symptoms facilitate earlier recognition and targeted management, whereas NT2's subtler presentation may contribute to delayed diagnosis and under-recognition, emphasizing the need for careful clinical evaluation.

Although our findings demonstrate consistent phenotypic differences between NT1 and NT2, the biological mechanisms underlying these distinctions remain incompletely understood [25,26]. The NT1 is strongly associated with hypocretin deficiency resulting from selective loss of hypocretin-producing neurons, likely mediated by autoimmune processes, which provides a well-established pathophysiologic explanation for its more severe, stable clinical phenotype [25,27]. In contrast, NT2 lacks consistent hypocretin deficiency and appears biologically heterogeneous. The proposed mechanisms include partial or fluctuating hypocretin dysfunction, involvement of alternative wake-promoting neurotransmitter systems, or dysregulation of arousal networks rather than complete neuronal loss [25]. Longitudinal studies further suggest that a subset of NT2 patients may subsequently develop cataplexy or biochemical features consistent with NT1, supporting the hypothesis that NT2 may, in some cases, represent an early or evolving form of NT1, while in others reflecting a distinct or heterogeneous condition [27,28,29]. This biological uncertainty likely contributes to the greater diagnostic instability, lower MSLT reproducibility, and more variable clinical presentation observed in NT2, and should be considered when interpreting phenotypic differences between narcolepsy subtypes.

In our cohort, the mean age at time of diagnosis was 28.9 ± 14.4 years, with an average diagnostic delay of 5.3 ± 3.0 years, which aligns with the reported literature of delays ranging from 5–15 years [12,13,18,19,20,21]. In the previous local study, a mean diagnostic delay of 8.4 ± 1.2 years among Saudi patients was reported, with a mean age at symptom onset of 20.5 ± 1.4 years [18]. Furthermore, large, European multi country analysis involving 580 patients with narcolepsy similarly highlight that prolonged delays remain pervasive, with a mean age of 30.5 years at diagnosis time and a diagnostic delay of 9.7 years [12]. This study revealed that this was influenced by referral pathways and variable recognition of hallmark symptoms, particularly when cataplexy was absent [12]. More broadly, sleep disturbances such as EDS, fragmented nocturnal sleep, and REM-related symptoms are frequently under-recognized or misattributed in routine clinical practice, often being mistaken for psychiatric, behavioral, or lifestyle-related conditions [30]. This under-recognition contributes substantially to delayed referral to sleep specialists and postponed diagnostic evaluation, a phenomenon consistently reported across the sleep-disorders literaturen [18,21,30]. Such diagnostic overshadowing is especially pronounced in patients with NT2, where the absence of cataplexy further complicates early recognition. Moreover, regarding sex distribution, our study demonstrated a slight male predominance (59.5%). Globally, epidemiologic work has not shown a consistent global predominance of either males or females [31,32]. However, a recent study indicated that women may experience longer diagnostic delays and more frequent misdiagnosis, even when they present with similar symptom profiles to those of men [33]. This study indicated that 85% of men were diagnosed after 16 years from symptom onset, compared to 28 years in women [33]. Therefore, enhancing clinician awareness (especially for NT2), standardizing referrals to sleep specialists, and employing objective testing may help narrow sex-related disparities and reduce the time to diagnosis.

Moreover, our PSG data revealed marked sleep disruption characterized by an elevated AI (15.7 ± 11.5 events/hour) and prolonged WASO (63.2 ± 51.9 min), indicating substantial sleep instability; however, no significant differences were observed between the 2 subtypes. These findings align with existing research that consistently reports fragmented nocturnal sleep in patients with narcolepsy [1,18,24,34,35]. Bahammam et al. [18] similarly reported impaired sleep continuity among Saudi patients, with NT1 patients experiencing poorer overall nocturnal sleep quality than NT2 patients did. Similarly, a large Japanese study of 118 newly diagnosed, untreated patients with narcolepsy reported elevated AI and WASO, with NT1 patients exhibiting significantly greater impairment than NT2 patients did [24]. Moreover, a recent meta-analysis comparing PSG parameters across narcolepsy types confirmed that compared with NT2 patients, NT1 patients demonstrate markedly increased WASO, AI, and percentage of light sleep [34]. In line with these observations, recent reviews have described frequent brief nocturnal awakenings and pervasive sleep fragmentation as clinical hallmarks of narcolepsy [1]. Thus, the evidence of sleep fragmentation in our cohort and other international cohorts underscores the paradox of “non-refreshing sleep” despite adequate or increased sleep duration. This illustrates that EDS in narcolepsy stems not from insufficient sleep but from a profoundly unstable sleep architecture.

The clinical relevance of disrupted sleep extends beyond nocturnal symptoms alone, as growing evidence suggests that sleep fragmentation is associated with broader functional and behavioral consequences. Recent systematic reviews and meta-analysis have shown that sleep disturbances are significantly linked to impaired psychological well-being and increased risk of suicidal ideation and attempts among otherwise healthy pediatric and adolescent populations, as well as individuals with psychiatric illness. underscoring the wide-ranging clinical implications of unstable sleep [36,37]. Although these populations differ from adults with narcolepsy, the overarching findings reinforce that fragmented sleep is not merely a nighttime phenomenon but may carry broader consequences for daytime functioning and well-being. Framing our findings within this broader context emphasizes the importance of recognizing and addressing sleep instability as a clinically meaningful aspect of narcolepsy management.

In addition, our study demonstrated that treatment led to a significant reduction in ESS scores, from 18.4 ± 4.2 to 9.2 ± 2.4 (p < 0.001), indicating a marked improvement in EDS. In the context of limited access to newer narcolepsy therapies in many regions (including pitolisant, solriamfetol, and sodium oxybate), modafinil remained the most frequently prescribed medication in our cohort (69%), followed by methylphenidate (16.7%) and a combination of modafinil and fluoxetine (14.3%). This prescribing pattern reflects real-world clinical practice in settings where availability, cost, and regulatory constraints influence treatment selection. These findings align with those of several studies, which have consistently demonstrated that modafinil effectively reduces EDS in patients with narcolepsy [16,38,39,40,41]. Moreover, a 6-week open-label study involving 151 patients previously treated with other stimulants demonstrated significant improvements in ESS scores from the first week of modafinil administration [39]. By the end of the study period, 79% of patients demonstrated clinical improvement, with modafinil showing minimal side effects compared with other drugs [39]. Similarly, a meta-analysis of randomized controlled trials (RCTs) confirmed that modafinil significantly improved ESS scores compared to placebo [40]. These studies support our findings and reinforce the role of modafinil in narcolepsy as a first-line treatment for EDS [38]. Consequently, modafinil has largely replaced traditional stimulants such as methylphenidate and amphetamine as the first-line therapy for EDS and sleep attacks based on RCT, despite the absence of head-to-head comparison trials [42]. Additionally, fluoxetine, a selective serotonin reuptake inhibitor (SSRI), has demonstrated mild efficacy in reducing cataplexy symptoms at doses ranging from 20 to 60 mg [43]. Collectively, these findings underscore the effectiveness of pharmacologic therapy in managing narcolepsy symptoms.

Despite the valuable findings of our study, it is necessary to acknowledge certain limitations. First, the retrospective design inherently introduces potential biases, including incomplete or inconsistent documentation in medical records. Second, the single-center setting may limit the generalizability of our findings to other regions or health care systems within KSA or the broader Middle East. Third, the relatively small sample size may restrict the statistical power to detect subtle differences between subgroups. Moreover, although objective measures such as PSG and MSLT were utilized, variability in test timing, patient adherence, and prior treatment exposure may have influenced the results. Additionally, CSF hypocretin-1 levels, which may sometimes help confirm the diagnosis in suspected cases, were not available for all patients because of resource constraints. Furthermore, follow-up posttreatment ESS data were collected via electronic surveys, which may introduce recall or reporting bias. Finally, although modafinil, methylphenidate, and fluoxetine were the main pharmacologic interventions, this study did not systematically evaluate long-term adherence, side effects, or comparative efficacy, limiting conclusions about optimal treatment strategies. Future prospective, multicenter studies with larger sample size and standardized longitudinal follow-up are warranted to validate these findings and provide more robust guidance for the management of narcolepsy in this region.

In conclusion, this study provides valuable insights into the clinical characteristics, PSG findings, and therapeutic outcomes of patients with narcolepsy in 1 of the tertiary academic centers in KSA. The NT1 was slightly more frequent and associated with more severe EDS and shorter sleep latencies. Diagnostic delays remain substantial, emphasizing the need for greater awareness and earlier recognition. The PSG demonstrated disrupted sleep continuity, whereas treatment, primarily with modafinil, was effective in reducing EDS. Despite the limitations inherent to the retrospective, single-center design, our study provides region-specific data that may guide clinicians to develop more advanced strategies that support early detection, individualized treatment, and improved long-term outcomes for patients with narcolepsy.

Acknowledgement

This research work was funded by Institutional Fund Projects under grant no (IFPRC-128-140-2020). Therefore, authors gratefully acknowledge technical and financial support from the Ministry of Education and King Abdulaziz University, Jeddah, Saudi Arabia.

Disclosure

This research work was funded by Institutional Fund Projects under grant no (IFPRC-128-140-2020). Ethical approval was obtained from the Unit of Biomedical Ethics at King Abdulaziz University Hospital. The study was conducted in accordance with the principles of the Declaration of Helsinki.

Disclosure statement

The authors confirm that no artificial intelligence (AI) tools were used in the writing, preparation, or editing of this manuscript, including the creation of text, figures, tables, or data analysis. The manuscript content, analyses, and interpretations presented are entirely the work of the authors. The authors confirm that this manuscript, in whole or in part, has not been previously published in any language, in print or online, and is not under consideration elsewhere.