Anxiety and depression symptoms mediate the impact of neuroticism on insomnia in adults with epilepsy: a cross-sectional study

Abstract

Objective

Comorbid insomnia is a common global occurrence among patients with epilepsy (PWE). Neuroticism could be a significant underlying factor for insomnia in this population. This study aimed to explore whether and how neuroticism, anxiety, and depressive symptoms interact and impact insomnia in PWE.

Methods

We recruited a continuous cohort of adult PWE. Demographic, clinical data, and information on neuroticism, anxiety, depression, and insomnia were collected. Assessments were conducted using the Eysenck Personality Questionnaire-Revised, Short Scale for Chinese (EPQ-RSC), Generalized Anxiety Disorder-7 (GAD-7), Neurological Disorders Depression Inventory for Epilepsy (NDDI-E), and Insomnia Severity Index (ISI). Process mediation analysis were employed to Investigate the relationships between neuroticism, anxiety, depression, and insomnia. Significant mediation effects were determined using the Bootstrap method with the SPSS PROCESS macro.

Results

We enrolled a total of 231 adult epilepsy patients in our study. Neuroticism demonstrated a significant positive association with symptoms of anxiety, depression, and insomnia. Neuroticism significantly predicted insomnia in patients. Anxiety symptoms and depressive symptoms exhibited multiple mediating effects between neuroticism and insomnia. Specifically, the direct effect of neuroticism on insomnia accounted for 40.20% of the total effect, while the indirect effects through anxiety symptoms and depressive symptoms, respectively, accounted for 31.52% and 28.28% of the total effect of neuroticism on insomnia.

Conclusions

Neuroticism, anxiety, and depressive symptoms are interrelated and associated with insomnia in patients with epilepsy. Partially mitigating the negative impact of neuroticism on insomnia by reducing the occurrence of anxiety and depressive symptoms may help reduce the risk of insomnia in PWE.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12883-025-04313-2.

Introduction

Epilepsy is a chronic neurological condition defined by repeated and unpredictable seizures, which significantly disrupt the sleep structure and efficiency of patients [1]. This results in a greater incidence of coexisting sleep disorders [2]. Earlier research has indicated that the frequency of sleep disorders in individuals with epilepsy is roughly twice as high as that in healthy people [3, 4]. Co-morbid sleep disorders can lead to problems related to interpersonal communication, memory, and cognitive functioning in patients with epilepsy, thus affecting their ability to socialize and learn [5]. Insomnia is the most common sleep-related symptom, affecting approximately half of these patients [6]. Numerous risk factors for comorbid insomnia in patients with epilepsy have been identified, including demographic variables such as low socioeconomic status, unemployment, divorce, and widowhood [7], epilepsy-related factors such as focal epilepsy, nocturnal seizures, and anti-seizure medication (ASM) polytherapy [8–10], and emotional factors like anxiety and depression [11]. Significantly, anxiety and depression are more powerful indicators of sleep disorders in PWE than factors related to epilepsy itself [10, 11].

Personality traits are regarded as the outcome of the interplay between genetic influences and environmental factors [12]. According to the Big Five model of personality, these traits are divided into five basic dimensions [13]. Of these, Neuroticism, which is characterized by difficulties in managing negative emotions, has been shown to be associated with insomnia. In the general population, individuals with high levels of neuroticism tend to exhibit high levels of alertness and poor sleep quality [14]. Previous studies have shown that this effect may be mediated through multiple physiological pathways. Based on the neuroendocrine system, individuals with high levels of neuroticism tend to exhibit hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis, leading to elevated levels of cortisol, which can directly interfere with the structure of sleep, leading to sleep fragmentation, reduced deep sleep, and shorter total sleep time [15, 16]. In addition, neuroticism may further disrupt sleep by affecting the brain’s arousal systems, such as the blue spot/norepinephrine system, to increase the frequency of arousals [17]. In terms of psychological mechanisms, neuroticism may indirectly affect sleep through excessive mind wandering and symptom rumination [18].

Notably, individuals with higher levels of neuroticism are more susceptible to negative emotions, such as anxiety, worry, fear, and depression, which are closely associated with reporting more somatic symptoms and psychological distress [13].Hyperactivation of the HPA axis and elevated cortisol levels often lead to anxiety and depressive disorders [19]. In addition, neuroticism has been associated with abnormal regulation of neurotransmitters such as serotonin, norepinephrine (NE), and dopamine (DA), and imbalances in these neurotransmitters not only exacerbate mood disorders, but also indirectly contribute to insomnia by affecting sleep regulation centers [20, 21]. Specifically, anxiety symptoms interfere with the induction and maintenance of sleep by increasing an individual’s excessive concern and worry about sleep problems and heightening alertness, whereas depressive mood leads to disruption of sleep architecture by decreasing an individual’s motivation and vigor, and affecting his or her ability to regulate sleep [22]. Thus, neuroticism is not only directly associated with anxiety and depression but may also indirectly affect sleep quality through these mood disorders, a complex interaction that is prevalent in the general population and has a profound impact on an individual’s mental health and quality of life.

In patients with epilepsy, neuroticism is not only a core personality trait but also closely associated with a variety of psychological and behavioral problems. Previous studies have found that patients with epilepsy have higher levels of neuroticism than healthy population [23]. High levels of neuroticism have been associated with feelings of shame, impaired quality of life, and suicidal ideation in patients with epilepsy [1, 24, 25]. Furthermore, there is growing evidence that neuroticism is the strongest predictor of anxiety and depression in patients with epilepsy, revealing distinct but overlapping patterns of abnormal functional connectivity associated with depressive and anxiety symptoms [23, 26]. More importantly, patients with epilepsy may exhibit psychological and sleep problems that are different from those of the general population owing to their unique pathophysiological mechanisms and psychosocial stresses. Repeated unpredictable seizures, chronic stress, and social discrimination further exacerbate the disease burden [27]. Although previous studies have explored the association between neuroticism and insomnia in the general population and in patients with specific psychiatric disorders, studies exploring the intrinsic links between these variables in a specific population of patients with epilepsy are still limited, and there is still a lack of empirical studies on the relationship between neuroticism and insomnia in the epilepsy population. Based on the above theories, we proposed the following hypothesis: neuroticism may be a key factor influencing insomnia in patients with epilepsy, and given its association with increased anxiety and depressive symptoms, the effect of neuroticism on insomnia in patients with epilepsy may be explained by mood mediation.

This study focuses on adult epilepsy patients, constructing a mediation model of neuroticism and insomnia with anxiety and depressive symptoms as mediators (see Fig. 1). The aims of this study are to ascertain: (a) the associations among neurotic personality, anxiety symptoms, depressive symptoms, and insomnia in adult epilepsy patients; (b) whether neurotic personality can predict insomnia in adult epilepsy patients; (c) whether neurotic personality indirectly influences insomnia through mediating variables (anxiety and depressive symptoms).

Fig. 1.

Mediating effect diagram. The coefficient c is the total effect between X and Y, and c'is the direct effect of X on Y whilst controlling for M1 and M2. All path coefficients are standardized. *p<0.05, ***p < 0.001

Materials and methods

Participants

We conducted a cross-sectional study and invited epilepsy patients receiving treatment at the neurology outpatient clinic of the First Affiliated Hospital of Chongqing Medical University to participate. The criteria for inclusion were as follows: (1) age ≥ 16 years; (2) the diagnosis of epilepsy was in accordance with the 2017 International League Against Epilepsy (ILAE) criteria [28, 29]; (3) stable regimen of ASMs for a minimum duration of one month; (4) sufficient literacy to complete the questionnaire; (5) Willingness to participate in the study and provide signed informed consent. Exclusion criteria included: (1) Serious neurological or psychiatric conditions, including aphasia, hemiplegia, schizophrenia, significant cognitive deficits, and personality disorders; (2) inability to understand or complete the questionnaire as assessed by a physician; (3) incomplete questionnaire. The research protocol received approval from the Ethics Committee of the First Affiliated Hospital of Chongqing Medical University (Ethics approval number: 2024-219-01), and all participants provided their signed informed consent.

Measures

During face-to-face interviews, structured questionnaires (Supplementary File 1) were used to collect sociodemographic and epilepsy-related clinical characteristics of the patients, with additional information gathered from medical records when necessary. The characteristics encompassed age, sex, Body Mass Index (BMI), occupation, educational attainment, age at onset of first seizure, epilepsy duration, seizure frequency over the past six months, epilepsy type, and ASM treatment regimen. Furthermore, participants completed a series of standardized self - report questionnaires [30–33]. The Eysenck Personality Questionnaire-Revised, Short Scale for Chinese (EPQ-RSC) [30] was used to assess the level of neuroticism among participants. The Generalized Anxiety Disorder-7 (GAD-7) [31] scale was employed to evaluate the severity of anxiety symptoms. The Neurological Disorders Depression Inventory for Epilepsy (NDDI-E) [32] was utilized to assess the severity of depressive symptoms. The Insomnia Severity Index (ISI) [33] was administered to investigate the presence and severity of insomnia symptoms among participants.

EPQ-RSC [30]

It was employed to evaluate the degree of neuroticism in patients. This questionnaire, developed by Professor Eysenck and others, was revised into a Chinese version by Mingyi Qian et al. [30]. The EPQ-RSC is designed for Chinese adults aged 16 years or older (including 16 years old). The Neuroticism subscale consists of 12 items, and participants only need to answer ‘yes’ or ‘no’, with a total score ranging from 0 to 12. A standardized T-score (T = 50 + 10*(X-M)/SD) was calculated based on the total score obtained to analyze the personality characteristics of the participants. T-scores between 43.3 and 56.7 were considered as intermediate, between 38.5 and 43.3 or 56.7–61.5 as trend, and below 38.5 or above 61.5 as typical [34]. In this study, the Cronbach’s alpha coefficient for the neuroticism subscale was 0.84.

GAD-7 [31]

Initially developed by Spitzer et al. [35]. It was validated in its Chinese version by Tong et al. [31]. It was utilized to quickly screen for anxiety symptoms over the past two weeks and to evaluate their severity. This scale uses a Likert 4-point rating system, ranging from “not at all” to “nearly every day,” scoring 0–3 points respectively across seven items. A GAD-7 score greater than 6 has been validated as a reliable and effective cutoff for identifying anxiety symptoms in Chinese epilepsy patients [31]. In this study, the Cronbach’s alpha coefficient for GAD-7 was 0.888.

NDDI-E [32]

It was developed by Gilliam et al. [36], and validated in a Chinese version by Tong et al. [32]. This self-rated scale uses a Likert 4-point rating system, ranging from “none” to “nearly every day,” scoring 1–4 points respectively across six items. The optimal threshold for severe depression varies across languages, but for the Chinese version, a 2019 meta-analysis suggested a score > 13 [37]. The NDDI-E demonstrated good internal consistency in this study, with a Cronbach’s alpha coefficient of 0.825.

ISI [33]

It was a self-report questionnaire developed by Morin et al. [38], and validated in a Chinese version by Yu et al., was employed to assess the severity of insomnia symptoms over the past two weeks [33]. The ISI consists of seven items [39]. The ISI total score spans from 0 to 28, with scores of 8 or above indicating the presence of insomnia symptoms and higher scores reflecting a more severe level of symptoms. In this study, the Cronbach’s alpha coefficient for the ISI was found to be 0.81.

Statistical analysis

IBM SPSS Statistics for Windows v.25.0 and the macro PROCESS v 4.1 [40, 41] were used for statistical analyses. We used mean ± SD to represent continuous variables and frequencies and percentages to express categorical variables. We used Spearman correlation analysis to evaluate the relationships among neuroticism (independent variable), anxiety symptoms (mediator 1), depressive symptoms (mediator 2), and insomnia (dependent variable). PROCESS v4.1 macro was used to analyze the mediating roles of anxiety and depressive symptoms in the relationship between neuroticism and insomnia. Moreover, to assess the indirect effects of each variable. A total of 5000 bootstrap samples were used to compute the 95% confidence intervals (CIs). If the 95% CI did not include zero, the indirect effect was deemed statistically significant.

Results

Demographic and clinical characteristics

Of the 250 participants in the study, 19 were excluded due to incomplete questionnaire responses, leaving 231 datasets for final analysis. The demographic and clinical characteristics are summarized in Table 1. The mean age of the patients was 36.03 years, comprising 48.1% males and 51.9% females. The majority of participants (63.6%) were not single, about half (54.1%) had full-time or part-time employment, and 66.6% had an education level of high school or above. The average age at the first epileptic seizure was 23.87 years. Most patients (89.2%) had focal epilepsy, half of the participants (51.5%) had a disease duration of ≤ 10 years and 52.8% were on monotherapy. Only 29.9% of patients had no seizures in the past six months. Among all patients, 34.6% had anxiety symptoms, 29.4% had depressive symptoms, and 42.9% had insomnia.

Table 1.

Demographic and clinical characteristics

Characteristics	Mean ± SD or n (%)
Age (years)	36.03 ± 12.83
Gender
Male	111 (48.1)
Female	120 (51.9)
BMI (kg/m2)	22.94 ± 3.73
Marital status
Single	84 (36.4)
Non-single	147 (63.6)
Educational level
Primary school and below	20 (8.7)
Junior high school	57 (24.7)
High school	56 (24.2)
University and above	98 (42.4)
Employment status
Students	21 (9.1)
Unemployed	66 (28.6)
Part-time job	19 (8.2)
Full-time job	106 (45.9)
Retired	19 (8.2)
Age at onset (years)	23.87 ± 14.65
Duration (years)
≤ 10 years	119 (51.5)
>10years	112 (48.5)
Seizure frequency
No seizure	69 (29.9)
<1time per month	83 (35.9)
≥ 1time per month	79 (34.2)
Epilepsy types
Focal epilepsies	206 (89.2)
Generalized epilepsies	25 (10.8)
ASMs
Monotherapy	122 (52.8)
Polytherapy	109 (47.2)
Anxiety symptoms	80 (34.6)a
Depression symptoms	68 (29.4)b
Insomnia	99 (42.9)c

N=231

SD Standard deviation

^aGAD-7＞6

^bNDDI-E＞13

^cISI ≥8

Correlation between the main study variables

The mean values, standard deviations, and Spearman correlations of the key research variables are shown in Table 2. The neuroticism dimension score on the EPQ-RSC was 53.30 ± 12.40, the total score on the GAD-7 was 5.31 ± 5.28, the total score on the CNDD-E was 10.70 ± 4.81, and the total score on the ISI was 7.50 ± 6.48. As expected, correlation analyses indicated positive relationships between neuroticism and anxiety symptoms (r = 0.716, p < 0.001), depressive symptoms (r = 0.705, p < 0.001), and insomnia (r = 0.500, p < 0.001). Moreover, there were significant positive associations between insomnia and anxiety (r = 0.504, p < 0.001), as well as between insomnia and depressive symptoms (r = 0.478, p < 0.001).

Table 2.

Spearman's correlations of the main study variables

Variables	Mean ± SD	1	2	3	4
1. Neuroticism	53.30 ± 12.40	1
2. Anxiety symptoms	5.31 ± 5.28	0.716***	1
3. Depression symptoms	10.70 ± 4.81	0.705***	0.772***	1
4. Insomnia	7.50 ± 6.48	0.500***	0.504***	0.478***	1

N=231

SD Standard deviation

***p < 0.001

Mediating effect of anxiety and depression symptoms

Based on correlation analyses, we employed Preacher and Hayes’ parallel mediation model (Model 4) to examine the mediating roles of anxiety and depressive symptoms between neuroticism and insomnia. We conducted mediation effect tests using bias-corrected percentile Bootstrap resampling 5000 times. The results (Table 3; Fig. 1) indicated that neuroticism significantly predicted anxiety symptoms (β = 0.695, p < 0.001), depressive symptoms (β = 0.681, p < 0.001), and insomnia (β = 0.495, p < 0.001). When all predictors were included simultaneously, neuroticism (β = 0.199, p < 0.05), anxiety symptoms (β = 0.224, p < 0.05), depressive symptoms (β = 0.206, p < 0.05) all significantly predicted insomnia.

Table 3.

Results of the multiple mediation analysis

Regression model outcome variable	Predictor variable	Goodness-of-Fit indices			Regression coefficient and significance
		R	R2	F	β	t
Insomnia	Neuroticism	0.495	0.245	74.269***	0.495	8.618***
Anxiety symptoms	Neuroticism	0.695	0.483	213.923***	0.695	14.626***
Depression symptoms	Neuroticism	0.681	0.464	198.364***	0.681	14.084***
Insomnia	Neuroticism	0.566	0.320	35.592***	0.199	2.475*
	Anxiety symptoms				0.224	2.459*
	Depression symptoms				0.206	2.303*

N=231

*p < 0.05,*** p < 0.001

The Bootstrap results (Table 4) revealed statistical significance for direct and indirect effects. The total effect of neuroticism on insomnia was significant (path c = 0.495, 95% Boot CI = 0.199, 0.318). The direct effect of neuroticism on insomnia accounted for 40.20% of the total effect (path c'=0.199, 95% Boot CI = 0.014, 0.212). Moreover, both anxiety and depressive symptoms served as multiple mediators between neuroticism and insomnia, with the total indirect effect (path a₁a₂b₁b₂ = 0.296, 95% Boot CI = 0.164, 0.421) comprising 59.80% of the total effect of neuroticism on insomnia. Anxiety symptoms (path a₁b₁ = 0.156, 95% Boot CI = 0.018, 0.303) and depressive symptoms (path a₂b₂ = 0.140, 95% Boot CI = 0.010, 0.264) accounted for 31.52% and 28.28% of the total effect, respectively.

Table 4.

Bootstrap analysis of multiple mediation effects

Effect	Effect size	SE	95% CI Boot CI Lower upper		Percentage of effects
Total effect	0.495	0.030	0.199	0.318	100%
Direct effect	0.199	0.042	0.014	0.212	40.20%
Indirect effect
Total	0.296	0.066	0.164	0.421	59.80%
X→M1→Y	0.156	0.072	0.018	0.303	31.52%
X→M2→Y	0.140	0.066	0.010	0.264	28.28%

N=231

Bootstrap = 5000; → = unidirectional path; X→M1→Y: Neuroticism→Anxiety symptoms→Insomnia; X→M2→Y: Neuroticism→Depression symptoms→Insomnia

Discussion

The objective of this study was to explore the connection between neuroticism and insomnia in individuals with epilepsy. Initially, we hypothesized that neuroticism in these individuals is a potentially significant factor for insomnia, with anxiety and depressive symptoms predicted to mediate this relationship. Our findings is the first to demonstrate that pairwise correlations among neuroticism, anxiety symptoms, depressive symptoms, and insomnia. Furthermore, through a mediation analysis model, we established that neuroticism can predict insomnia in adults with epilepsy, emphasizing the significant influence and mediating roles of anxiety and depressive symptoms in the relationship between neuroticism and insomnia in people with epilepsy.

In previous cross-sectional studies on people with epilepsy, the prevalence of insomnia varied greatly, ranging from 14.4 to 85% based on the ISI [9, 42]. This variation could be attributed to factors such as participant selection, types of antiepileptic drugs, and differing cut-off values for diagnosing clinically relevant insomnia. In our study, we observed a high prevalence (42.9%) of comorbid insomnia in adults with epilepsy, consistent with prior research [43]. This may be attributed to the fact that epileptic seizures frequently happen during sleep, disturbing the sleep microstructure and impeding the transition from light to deep sleep stages, which results in trouble falling asleep, decreased sleep quality, and sleep structure disorders [44, 45]. Simultaneously, long-term use of antiepileptic drugs may further disrupt neuroendocrine function and neurotransmitter homeostasis, which are essential for maintaining normal sleep patterns [46]. Together, these factors lead to a significantly higher incidence and severity of insomnia in epilepsy patients. In addition to physical stressors, people with epilepsy are chronically exposed to the multifaceted psychosocial pressures of the disease. Fear of seizures and concerns about quality of life keep them in a chronic state of stress and make them more prone to mood disorders, such as anxiety and depression [27]. Despite geographic and methodological differences, previous studies have shown that insomnia is more common in patients with epilepsy and may lead to poor seizure control, exacerbate mood disorders, such as anxiety and depression, and significantly reduce patients’ quality of life [47, 48]. Given the detrimental effects of insomnia on both physical and mental health, as well as the increased demand for healthcare services, addressing insomnia is crucial in the comprehensive management of epilepsy.

The link between neuroticism and insomnia has been recognized in the general population [14]. However, empirical studies on the correlation between these factors are still lacking in specific groups of patients with epilepsy. Our study demonstrated a positive predictive effect of neuroticism on insomnia in patients with epilepsy for the first time, suggesting that higher levels of neuroticism may be associated with more severe insomnia symptoms. Among various personality traits, neuroticism is the strongest predictor of poor sleep quality [49]. In individuals with epilepsy, this relationship is complex and may be influenced by multiple factors. Individuals with high levels of neuroticism are usually in a state of hypervigilance, more responsive to stimuli from environmental changes, more sensitive to sleep disruptions caused by abnormal neuronal discharges in the brain, and more likely to experience negative emotions such as anxiety, worry, fear, and depression, which can lead to hyperarousal and increased susceptibility to insomnia [50]. Additionally, epilepsy patients may have low gamma-aminobutyric acid (GABA) levels or abnormal GABA receptor function, which can interfere with normal sleep regulation [51]. Moreover, during and after seizures, the HPA axis may be overactivated in patients with epilepsy, leading to elevated cortisol levels, which in turn interfere with the sleep-wake cycle and increase the frequency of awakening, leading to insomnia [51]. Individuals with high levels of neuroticism also exhibit similar physiological characteristics, with abnormalities in the activity of the autonomic nervous system and neuroendocrine system, which may interact with the stress of the disease itself to further exacerbate insomnia [15, 17]. In addition, individuals with high levels of neuroticism have abnormal brain activity, as evidenced by enhanced amygdala activity [52]. This abnormal brain activity may interact with structural and functional changes in the brain during seizures, leading to the excessive arousal of emotional responses and exacerbation of insomnia in people with epilepsy.

Anxiety and depressive symptoms are common in PWE. Our study reveals prevalence rates of 34.6% for anxiety symptoms and 29.4% for depressive symptoms. A previous study on adult PWE in Canada reported prevalence rates of 23% and 33% for anxiety and depression respectively [53], similar to the rates observed in our sample. Furthermore, past research has confirmed that neuroticism is the strongest predictor of anxiety and depression in PWE, displaying distinct and overlapping abnormal functional connectivity patterns with depressive and anxiety symptoms [23, 26]. Individuals with higher levels of neuroticism show stronger emotional responses to stimuli, especially negative events, adopt a negative perspective on daily life events, tend to perceive them as threatening, and rely on maladaptive coping strategies such as worrying and ineffective avoidance strategies, which in turn leads to high neuroticism individuals experiencing more negative emotions such as anxiety, worry, fear, and depression [13]. Our results reaffirm this association, with neuroticism significantly predicting anxiety and depressive symptoms in adult PWE.

According to our analysis, we found that anxiety and depressive symptoms are related to insomnia in PWE and significantly predict insomnia, aligning with previous research. For instance, Jo et al. carried out a cross-sectional study involving 126 epilepsy patients and discovered a correlation between the insomnia severity index and scores for anxiety and depression [54]. Moreover, a study on the correlation between sleep disorders and affective symptoms in Chinese adult PWE found that after controlling for epilepsy-related factors, depressive and anxiety symptoms were significant predictors of the Insomnia Severity Index scores [11]. This indicates that anxiety and depressive symptoms are independently linked to comorbid insomnia in PWE. Additionally, a recent investigation into the relationship between epilepsy and sleep disorders in American adults observed that depressive symptoms accounted for approximately 23.0 to 26.5% of the association between epilepsy and sleep disorders, offering deeper insights into the connection between emotions and sleep [45].

Notably, our mediation analyses indicated that anxiety and depressive symptoms significantly mediate the relationship between neuroticism and insomnia in adult patients with epilepsy. To be specific, the direct impact of neuroticism on insomnia made up 40.20% of the overall effect, whereas the indirect impacts of anxiety and depressive symptoms accounted for 31.52% and 28.28% of the total effect, respectively. This suggests that anxiety and depressive symptoms play independent roles in the relationship between neuroticism and insomnia. Studies conducted in the general population have shown that individuals with high levels of neuroticism are more sensitive to stressful life events, tend to amplify stress and hyperfocus in the external environment, and have poor emotion regulation, leading to significant anxiety and depression, and an increased risk of insomnia [49, 55, 56]. In adult patients with epilepsy, our study further revealed that high neuroticism levels increased the risk of insomnia by increasing the prevalence of anxiety and depressive symptoms. The occurrence of anxiety symptoms enhances an individual’s preoccupation with and worries about negative sleep-related events, leading them to overthink the negative effects of insomnia, which can further exacerbate insomnia symptoms [56]. Depressive symptoms, on the other hand, may reduce patients’ ability to regulate their mood and overall life satisfaction, a mood state that makes it more difficult for them to recover from sleep disruption, which in turn leads to a decrease in the quality of their sleep and exacerbates the effects of neuroticism on insomnia [22]. This finding is significant because it provides new insights into the underlying mechanisms of insomnia in patients with epilepsy, and provides an important basis for early personality assessment at the time of epilepsy diagnosis to predict insomnia risk in the clinic. More importantly, this study suggests the importance of early detection and treatment of depression and anxiety, which allows for early and timely intervention in people at a high risk for insomnia. Although it is challenging for clinicians to reduce patients’ neuroticism levels, interventions for anxiety and depression are widely available, such as early patient education and psychological interventions. Improving a patient’s mood state by reducing the prevalence of anxiety and depression may partially reduce the negative impact of neuroticism on insomnia, and thus may help reduce the risk of insomnia.

Several limitations of our study should be noted. First, the cross-sectional design of this study only reflected the association of variables at a specific point in time. Future studies could use a longitudinal design to more accurately reveal the causal relationship and dynamic process of change among these variables. Second, we only examined neuroticism; a more comprehensive understanding of how personality traits influence epilepsy patients may necessitate further research on all five traits. Furthermore, our sample was drawn from a single center and all from tertiary hospitals, where patients may experience more severe epilepsy attacks than those treated in primary clinics, thus not fully representing the entire epilepsy population. Although there was a significant correlation between anxiety and depression, the parallel mediation model did not test the moderating effects between them, and these interactions may affect the path and strength of their effects on insomnia. The use of more complex statistical models may be considered in the future to explore the dynamic relationship between variables in depth. Finally, our assessments of personality, mood, and sleep were based on patient self-assessment scales, which are subjective and may have potential reporting bias due to the lack of objective measures, such as activity loggers or polysomnographic monitoring. These limitations should be addressed in future research.

Conclusion

In summary, this study developed a theoretical model exploring the relationships among neuroticism, anxiety symptoms, depressive symptoms, and insomnia in PWE. Notably, this research is the first to demonstrate that neuroticism predicts insomnia in this population, with the mediating roles of anxiety and depressive symptoms also confirmed. This suggests a new possibility that the negative effect of neuroticism on insomnia can be partially reduced by decreasing the incidence of anxiety and depression, which may help reduce the risk of insomnia in people with epilepsy. These findings are significant as they provide new insights into the interplay between neuroticism and insomnia, offering valuable methods and a theoretical framework for preventing insomnia in PWE.

Authors’ contributions

Pan Hu conceptualized the research, conducted the preliminary analysis, and drafted the initial manuscript. Zheng Xiao and Xuefeng Wang reviewed and revised the manuscript. Pan Hu, Yu Han and Kairui Li were responsible for data collection. All authors read and approved the final manuscript.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Data availability

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Declarations

Ethics approval and consent to participate

We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines. The study protocol was approved by the Ethics Committee of the First Affiliated Hospital of Chongqing Medical University (Ethics approval number: 2024-219-01). This research was carried out in accordance with the Declaration of Helsinki, and all participants signed an informed consent form.

Consent for publication

Not Applicable.

Competing interests

The authors declare no competing interests.