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Insomnia in personality disorders and substance use disorders
Journal Pre-proof Insomnia in personality disorders and substance use disorders T. Provencher, A. Lemyre, A Valli`eres, C.H. Bastien
PII:
S2352-250X(19)30184-8
DOI:
https://doi.org/10.1016/j.copsyc.2019.10.005
Reference:
COPSYC 956
To appear in:
Current Opinion in Psychology
Please cite this article as: Provencher T, Lemyre A, Valli`eres A, Bastien CH, Insomnia in personality disorders and substance use disorders, Current Opinion in Psychology (2019), doi: https://doi.org/10.1016/j.copsyc.2019.10.005
This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Published by Elsevier.
Insomnia in personality disorders and substance use disorders
Provencher, T. 1 , Lemyre, A. 1, Vallières, A. 1,2,3,4 Bastien, C.H., 1-2-5
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1. School of Psychology, Université Laval, Québec, QC, Canada 2. CERVO Brain research center, Québec, QC, Canada 3. Psycho | Socio | Cultural Sleep Laboratory, School of Psychology, Université Laval, Québec, QC, Canada 4. CHU Research Center - Université Laval, Québec, QC, Canada 5. Research Laboratory on Human Neurophysiology and Sleep, School of psychology, Université Laval, Québec, QC, Canada
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Corresponding author : Célyne H. Bastien, School of Psychology, Laval University, Quebec, QC, Canada, G1V0A6, e-mail: [email protected]; tel: 418-656-2131, ext 408344
Summary The relationship between certain personality disorders (PDs) and insomnia has been the object of few studies in recent years. Even though it is not indicated to use polysomnography to diagnose insomnia, objective measures have shown sleep abnormalities in individuals with a personality disorder and insomnia. Interestingly, there is increasing evidence that emotion dysregulation is involved in a mutually aggravating relationship between Borderline Personality Disorder
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(BPD) and insomnia. While BPD traits are highly associated with suicide ideation and attempts, these behaviors could be potentiated or enhanced in individuals
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presenting sleep disturbances. Because BPD and other mental disorders are
often linked with the use of medication or other substances, it is also important to review the association between substance use disorders (SUD) and insomnia.
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SUD can disrupt sleep and foster insomnia, which in turn might increase motivation to use substances. Insomnia has also been shown to precede (i.e.,
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predict) SUD, and can be present during withdrawal as well. These results
present a PD or SUD.
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highlight the need to assess and treat insomnia when working with patients who
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Keywords: insomnia; personality disorders; Addiction; CBT-I
Insomnia in personality disorders and substance use disorders Introduction Insomnia is an important health issue [1], afflicting around 10% of the general population [2]. It is associated with daily cognitive impairments (e.g., memory/attention deficits) [3] and higher rates of depression and anxiety [4]. The DSM-5 [5] defines insomnia as a difficulty in initiating or maintaining sleep which
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is present at least three times a week in the past three months based on subjective reports [5]. It can present itself alone or in comorbidity with another
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health disorder (mental, physical, or sleep-related). This paper will focus on
insomnia in comorbidity with personality disorders and substance use disorders
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since research in these particular areas has surged in recent years. 1. Personality disorders (PDs)
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1.1. Comorbidity between PDs and insomnia. A growing field of research focuses on the relationship between insomnia and PDs. Studies show that 50%
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to 93% of individuals with a PD experience at least one sleep problem or selfidentify as insomnia sufferers [6-8]. Conversely, more than 50% of individuals with insomnia received at least one PD diagnosis [9](*). These findings indicate
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that, while individuals with a PD are more likely to present sleep disturbances, individuals with insomnia may be at higher risk for exhibiting maladaptive personality traits. Since individuals with PDs suffer from high rates of Axis I disorders, there is a need to better determine specific relations between
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personality pathology and insomnia. In that regards, some studies control for Axis I pathology, but others do not. Documenting the relationship between PD and insomnia might enhance treatment efficacy for both sleep disturbances and maladaptive personality traits. 1.2. Borderline Personality Disorder (BPD) and insomnia. The published literature on sleep disorders and PDs focuses almost exclusively on BPD. In a large sample of older adults, the composite scores for all ten DSM-IV personality
disorders were positively associated with the presence of insomnia symptoms, but only BPD remained a significant correlate after controlling for covariates such as major depression, body-mass index, race, and gender [10]. 1.2.1. Sleep phenotype in individuals with a BPD. Individuals with a BPD exhibit signs of hyperarousal both during the day (e.g. daytime rumination) and night (e.g., difficulty falling asleep, frequent awakenings) [7]. Two weeks of sleep diaries showed that the sleep variables (i.e. increased sleep onset latency, low
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sleep efficiency) of individuals with a BPD and individuals with insomnia are
similar [11]. In the same line, a meta-analysis showed that individuals with a BPD
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spend more time awake (i.e. increased wake after sleep onset) and less time sleeping (i.e. decreased total sleep time) than healthy controls [12](*).
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1.2.2. Linking BPD and insomnia: the emotion dysregulation hypothesis. Sleep, and particularly rapid eye movement (REM) sleep, appears to play a role
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in emotion regulation [13,14]. Insomnia is likely to disturb this process since it can result in sleep deprivation or REM sleep fragmentation. In individuals with
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insomnia, emotion dysregulation has been linked to cognitive arousal (i.e. repetitive thinking, rumination) throughout the 24-h period. This form of cognitive arousal may in turn promote the perpetuation of sleep disturbances [15]. This
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likely bidirectional relationship may explain the strong link observed between insomnia and emotion dysregulation [15,16]. Emotion dysregulation is a core feature of BPD [5]. Therefore, it is possible that emotion dysregulation in individuals with BPD promotes cognitive arousal, and
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consequently, insomnia [17]. In turn insomnia would disturb the emotional regulation function of sleep, promoting BPD symptoms during wakefulness. Thus, there might be a mutually aggravating relationship between BPD and insomnia.
1.2.3. BPD, insomnia, and the risk for suicide. Research indicates that patients with BPD and comorbid sleep disturbances may be at increased risk for suicidality [18,19]. Precisely, the association between BPD traits and the risk of
suicide is mediated by symptoms of insomnia [18](*), indicating that suicide risk in individuals with a BPD increases when sleep disturbances are more severe. In this regard, it is known that individuals with insomnia exhibit sleep-related concerns [17]. These concerns can foster emotional distress, increasing the risk of a suicide attempt [18]. 1.3. Obsessive-compulsive personality disorder (OCPD) and insomnia. The evidence on the association between OCPD and insomnia is mixed. While one
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study did not find OCPD to be a significant correlate of insomnia after controlling
for covariates [10], another study [20] suggested that OCPD and/or sub-threshold
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features of this disorder may co-occur with chronic insomnia and poor sleep quality to a greater extent than other PDs. Although OCPD is not formally
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associated with emotional difficulties according to DSM-5 diagnostic criteria [5], it may nevertheless be associated with a difficulty in regulating negative emotions
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[21]. Thus, it is not surprising that the subjective sleep pattern of individuals with an OCPD exhibit peculiarities similar to those observed in individuals with a BPD. Specifically, individuals with features of OCPD exhibit an altered sleep pattern
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(i.e. increased wake time and number of awakenings, decreased sleep time and sleep efficiency) compared to controls [22].
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1.4. Antisocial personality disorder (APD) and insomnia. Maladaptive personality traits (machiavellianism, narcissism, and psychopathy) often seen in Cluster B personality disorders such as APD [23] are thought to disturb sleep through adverse cognitive-emotional processes (i.e. worry, rumination, poor coping mechanisms, and diminished emotion regulation) [24,25]. Furthermore,
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Van Veen et al. [26] found that poor sleep is common in forensic inpatients with an APD or a BPD, and that sleep problems are significantly related to self-reported impulsivity. It is hypothesized that individuals with already poor impulse control such as those with APD or BPD could be more vulnerable to the detrimental effects of sleep loss on inhibition [6]. Indeed, important difficulty falling asleep or short duration of sleep (< 5 h) may exacerbate impulsivity and/or psychiatric symptoms [8].
1.5. PDs and insomnia: clinical implications and future directions. There is a need to better understand the mechanisms underlying the relationship between BPD and insomnia. As of now, emotion dysregulation appears to play a role in mutually reinforcing psychological symptoms in these disorders, but available empirical evidence remains scarce. Developing and testing a theoretical model of the co-occurrence between PDs and sleep difficulties could be the target of future research. Such model might help in developing an integrated treatment. Future studies should also examine the unique relation between insomnia and
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other DSM-5 personality disorders. These studies may further highlight the need for clinicians to adapt their treatment approach with these patients. In the short
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term, we recommend that clinicians screen for the presence of sleep problems when evaluating patients with a PD and consider the possibility of treating
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insomnia. Conversely, maladaptive personality traits could be assessed before
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treating insomnia.
Finally, researchers should also document the use of medication or other substances which might interfere with treatment efficacy or potentiate sleep
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problems in any mental disorder (e.g. worsening sleep). This area is often overlooked in current research, especially when substance abuse disorders are
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present.
2. Substance use disorder (SUD) 2.1. Comorbidity between SUD and insomnia. Systematic and narrative literature reviews indicate that the use of substances and sleep disorders share a
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bidirectional relationship [27-29]. Insomnia can be present before substance dependence or abuse, or be associated with withdrawal (lasting for weeks) and relapse [27]. In their literature review, Grau-López et al. [30] reported that in studies recruiting patients with a SUD, the prevalence of insomnia ranges from 30% to 85% depending on the primary substance of abuse. Conversely, Dolsen et al. [31](*) found that individuals with a lifetime history of insomnia symptoms
used substances (i.e. alcohol, cocaine, and heroin) more frequently than good sleepers. 2.2. Substance use as a risk factor for sleep impairments. Chronic substance use severely affects the duration and quality of sleep, and these deleterious effects can also be observed during withdrawal [32]. Indeed, although the effect is dose-dependent, most drugs impact the amount of time spent in the different stages of sleep or the timing of NREM and REM sleep cycles, as well as both the
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subjective and objective quality and quantity of sleep [32-35]. In a review by
Chakravorty et al. [33](*), the most frequent sleep-related complaints in patients
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with SUD (i.e. alcohol, opioids, cannabis, cocaine, or sedative-hypnotic-anxiolytic drugs) included increased sleep latency and time awake after sleep onset.
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Recent studies have analyzed the effect of specific drugs, benzodiazepines (BZD) and opioids, on sleep. In one study [36], the long-term use of high doses
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of BZD for the treatment of chronic insomnia decreased slow wave brain activity. Regarding the effects of opioids, a single dose can improve subjective sleep
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quality in patients with chronic pain and insomnia [33], while it significantly alters sleep architecture in healthy adults [27]. Angarita et al. [27] reported that chronic or long-term use of opioids may lead to self-reported sleep dysfunction such as
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increased sleep latency, increased awakening, decreased total sleep time, and decreased sleep efficiency.
2.3. Insomnia as a risk factor for substance abuse. Drugs or alcohol can be used as self-medication attempts to facilitate sleep or to reduce the physical and
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emotional burden resulting from sleep difficulties [31,37]. In a sample of individuals with insomnia, the severity of insomnia was related to a higher likelihood of using cocaine at 12-months post-treatment, possibly as an attempt to alleviate a withdrawal-induced rebound in insomnia [31]. Furthermore, in a placebo controlled experiment, Roehrs and Roth [29] have shown that individuals with insomnia are at higher risk of substance abuse if they exhibit autonomic (i.e. elevated daytime urinary norepinephrine levels) or behavioral signs of
hyperarousal (i.e. higher nap sleep latency). From a clinical standpoint, this result suggests that reducing daytime hyperarousal in individuals with insomnia may prevent self-medication attempts. 2.4. Insomnia during withdrawal. While the effects of chronic long-term use of various drugs and substances on sleep have been investigated, withdrawal symptoms may have been neglected. In a review [38] on the effects of cannabis withdrawal on sleep, when abstaining from cannabis use, at least one third of
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participants reported experiencing trouble sleeping, strange dreams and waking up early, as well as a self-reported reduction insleep duration. Furthermore,
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sedative-hypnotic-anxiolytic drugs (including BZD and non-BZD) are often
prescribed to facilitate sleep [33]. However, abrupt cessation of these drugs,
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especially BZD, has been associated with sleep complaints such as decreased total sleep time and a poor sleep quality [33]. Indeed, attempting to quit
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sedative-hypnotic-anxiolytic drugs such as BZD may result in “rebound insomnia” (i.e. exacerbation of sleep disturbances) that may be even worse than before the use of the medication [39]. Encouragingly, studies found that intensive
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psychosocial support [40] or Cognitive Behavioral Therapy for Insomnia (CBT-I) [41] may markedly improve sleep and quality of life in older adults with primary
drugs.
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insomnia during withdrawal from long‐term use of sedative-hypnotic-anxiolytic
2.5. SUD and insomnia: clinical implications and future directions. There is strong evidence supporting the bidirectional relationship between SUD and insomnia [42]. While substance use is known to impact sleep, notwithstanding
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the substance, insomnia symptoms seem to contribute to the development and maintenance of SUD. Furthermore, there is growing but limited evidence on the effectiveness of insomnia treatment in patients with SUD [41,43,44]. In individuals with insomnia comorbid with another psychiatric condition (e.g., SUD), objective and subjective sleep quality can be fostered with CBT-I beyond the effect of pharmacotherapy [41,45]. Notably, CBT-I may include an optional module for discontinuing hypnotic medications [41], the tapering being
supervised by a physician. Thus, another area of research would be to examinetreatments that specifically target sleep disturbances in the context of withdrawal in individuals with a SUD. From a clinical perspective, when working with patients who present a SUD and insomnia, clinicians should be aware that these conditions are both linked to suicidality. Indeed, substance use (except LSD and psychedelic drugs [46]) is linked to suicidal ideation and attempts [47], as is insomnia [48]. More
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precisely, the risk of suicide is almost 18 times higher in insomnia than in non-insomnia populations [49]. Still, very few studies have tied insomnia,
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substance abuse, and suicide risk in the same predictive model [50]. Thus, future research may assess the possible additivity in the risk of suicide in individuals
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who present a SUD and insomnia compared to those who only present one of these disorders. Moreover, researchers have suggested that we identify
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individuals with a SUD who are at-risk for future relapse and who present comorbid sleep complaints to better inform prevention and intervention efforts, in
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the hope of also reducing the risk of suicide [37]. Conclusion
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Only a paucity of research exists in the field of personality disorders and insomnia. The relationship between substance use disorder and insomnia, on the other hand, has received more attention. Although the study of objective sleep is not recommended for the diagnosis of insomnia, this approach has highlighted peculiarities in the sleep of individuals with a PD or a SUD. For instance,
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individuals with a BPD present increased sleep onset latency and lower sleep efficiency. Importantly, emotion dysregulation appears to promote a mutually aggravating relationship between insomnia and BPD. In individuals with a SUD, insomnia can be present during periods of substance abuse and/or during withdrawal. Moreover, insomnia can increase the risk of relapse. This review highlights that insomnia is part of many personality disorders and substance use disorders in addition to be linked to suicidal ideation. Thus, from a transdiagnostic perspective, targeting insomnia during treatment can be a
promising avenue to increase the general well-being of individuals presenting these psychological difficulties. Randomized control studies targeting comorbid PDs and SUD in association with insomnia are needed to document the contribution of these respective disorders on sleep difficulties and vice-versa. Alternatively, taking a precision medicine approach could be ideal since the clinical picture of comorbid disorders is often complex. Dissemination of treatment efficacy and how to maintain therapeutic gains would be beneficial for
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all.
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None of the authors have any conflict of interests.
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PII:
S2352-250X(19)30184-8
DOI:
https://doi.org/10.1016/j.copsyc.2019.10.005
Reference:
COPSYC 956
To appear in:
Current Opinion in Psychology
Please cite this article as: Provencher T, Lemyre A, Valli`eres A, Bastien CH, Insomnia in personality disorders and substance use disorders, Current Opinion in Psychology (2019), doi: https://doi.org/10.1016/j.copsyc.2019.10.005
This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Published by Elsevier.
Insomnia in personality disorders and substance use disorders
Provencher, T. 1 , Lemyre, A. 1, Vallières, A. 1,2,3,4 Bastien, C.H., 1-2-5
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1. School of Psychology, Université Laval, Québec, QC, Canada 2. CERVO Brain research center, Québec, QC, Canada 3. Psycho | Socio | Cultural Sleep Laboratory, School of Psychology, Université Laval, Québec, QC, Canada 4. CHU Research Center - Université Laval, Québec, QC, Canada 5. Research Laboratory on Human Neurophysiology and Sleep, School of psychology, Université Laval, Québec, QC, Canada
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Corresponding author : Célyne H. Bastien, School of Psychology, Laval University, Quebec, QC, Canada, G1V0A6, e-mail: [email protected]; tel: 418-656-2131, ext 408344
Summary The relationship between certain personality disorders (PDs) and insomnia has been the object of few studies in recent years. Even though it is not indicated to use polysomnography to diagnose insomnia, objective measures have shown sleep abnormalities in individuals with a personality disorder and insomnia. Interestingly, there is increasing evidence that emotion dysregulation is involved in a mutually aggravating relationship between Borderline Personality Disorder
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(BPD) and insomnia. While BPD traits are highly associated with suicide ideation and attempts, these behaviors could be potentiated or enhanced in individuals
ro
presenting sleep disturbances. Because BPD and other mental disorders are
often linked with the use of medication or other substances, it is also important to review the association between substance use disorders (SUD) and insomnia.
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SUD can disrupt sleep and foster insomnia, which in turn might increase motivation to use substances. Insomnia has also been shown to precede (i.e.,
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predict) SUD, and can be present during withdrawal as well. These results
present a PD or SUD.
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highlight the need to assess and treat insomnia when working with patients who
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Keywords: insomnia; personality disorders; Addiction; CBT-I
Insomnia in personality disorders and substance use disorders Introduction Insomnia is an important health issue [1], afflicting around 10% of the general population [2]. It is associated with daily cognitive impairments (e.g., memory/attention deficits) [3] and higher rates of depression and anxiety [4]. The DSM-5 [5] defines insomnia as a difficulty in initiating or maintaining sleep which
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is present at least three times a week in the past three months based on subjective reports [5]. It can present itself alone or in comorbidity with another
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health disorder (mental, physical, or sleep-related). This paper will focus on
insomnia in comorbidity with personality disorders and substance use disorders
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since research in these particular areas has surged in recent years. 1. Personality disorders (PDs)
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1.1. Comorbidity between PDs and insomnia. A growing field of research focuses on the relationship between insomnia and PDs. Studies show that 50%
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to 93% of individuals with a PD experience at least one sleep problem or selfidentify as insomnia sufferers [6-8]. Conversely, more than 50% of individuals with insomnia received at least one PD diagnosis [9](*). These findings indicate
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that, while individuals with a PD are more likely to present sleep disturbances, individuals with insomnia may be at higher risk for exhibiting maladaptive personality traits. Since individuals with PDs suffer from high rates of Axis I disorders, there is a need to better determine specific relations between
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personality pathology and insomnia. In that regards, some studies control for Axis I pathology, but others do not. Documenting the relationship between PD and insomnia might enhance treatment efficacy for both sleep disturbances and maladaptive personality traits. 1.2. Borderline Personality Disorder (BPD) and insomnia. The published literature on sleep disorders and PDs focuses almost exclusively on BPD. In a large sample of older adults, the composite scores for all ten DSM-IV personality
disorders were positively associated with the presence of insomnia symptoms, but only BPD remained a significant correlate after controlling for covariates such as major depression, body-mass index, race, and gender [10]. 1.2.1. Sleep phenotype in individuals with a BPD. Individuals with a BPD exhibit signs of hyperarousal both during the day (e.g. daytime rumination) and night (e.g., difficulty falling asleep, frequent awakenings) [7]. Two weeks of sleep diaries showed that the sleep variables (i.e. increased sleep onset latency, low
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sleep efficiency) of individuals with a BPD and individuals with insomnia are
similar [11]. In the same line, a meta-analysis showed that individuals with a BPD
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spend more time awake (i.e. increased wake after sleep onset) and less time sleeping (i.e. decreased total sleep time) than healthy controls [12](*).
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1.2.2. Linking BPD and insomnia: the emotion dysregulation hypothesis. Sleep, and particularly rapid eye movement (REM) sleep, appears to play a role
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in emotion regulation [13,14]. Insomnia is likely to disturb this process since it can result in sleep deprivation or REM sleep fragmentation. In individuals with
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insomnia, emotion dysregulation has been linked to cognitive arousal (i.e. repetitive thinking, rumination) throughout the 24-h period. This form of cognitive arousal may in turn promote the perpetuation of sleep disturbances [15]. This
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likely bidirectional relationship may explain the strong link observed between insomnia and emotion dysregulation [15,16]. Emotion dysregulation is a core feature of BPD [5]. Therefore, it is possible that emotion dysregulation in individuals with BPD promotes cognitive arousal, and
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consequently, insomnia [17]. In turn insomnia would disturb the emotional regulation function of sleep, promoting BPD symptoms during wakefulness. Thus, there might be a mutually aggravating relationship between BPD and insomnia.
1.2.3. BPD, insomnia, and the risk for suicide. Research indicates that patients with BPD and comorbid sleep disturbances may be at increased risk for suicidality [18,19]. Precisely, the association between BPD traits and the risk of
suicide is mediated by symptoms of insomnia [18](*), indicating that suicide risk in individuals with a BPD increases when sleep disturbances are more severe. In this regard, it is known that individuals with insomnia exhibit sleep-related concerns [17]. These concerns can foster emotional distress, increasing the risk of a suicide attempt [18]. 1.3. Obsessive-compulsive personality disorder (OCPD) and insomnia. The evidence on the association between OCPD and insomnia is mixed. While one
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study did not find OCPD to be a significant correlate of insomnia after controlling
for covariates [10], another study [20] suggested that OCPD and/or sub-threshold
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features of this disorder may co-occur with chronic insomnia and poor sleep quality to a greater extent than other PDs. Although OCPD is not formally
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associated with emotional difficulties according to DSM-5 diagnostic criteria [5], it may nevertheless be associated with a difficulty in regulating negative emotions
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[21]. Thus, it is not surprising that the subjective sleep pattern of individuals with an OCPD exhibit peculiarities similar to those observed in individuals with a BPD. Specifically, individuals with features of OCPD exhibit an altered sleep pattern
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(i.e. increased wake time and number of awakenings, decreased sleep time and sleep efficiency) compared to controls [22].
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1.4. Antisocial personality disorder (APD) and insomnia. Maladaptive personality traits (machiavellianism, narcissism, and psychopathy) often seen in Cluster B personality disorders such as APD [23] are thought to disturb sleep through adverse cognitive-emotional processes (i.e. worry, rumination, poor coping mechanisms, and diminished emotion regulation) [24,25]. Furthermore,
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Van Veen et al. [26] found that poor sleep is common in forensic inpatients with an APD or a BPD, and that sleep problems are significantly related to self-reported impulsivity. It is hypothesized that individuals with already poor impulse control such as those with APD or BPD could be more vulnerable to the detrimental effects of sleep loss on inhibition [6]. Indeed, important difficulty falling asleep or short duration of sleep (< 5 h) may exacerbate impulsivity and/or psychiatric symptoms [8].
1.5. PDs and insomnia: clinical implications and future directions. There is a need to better understand the mechanisms underlying the relationship between BPD and insomnia. As of now, emotion dysregulation appears to play a role in mutually reinforcing psychological symptoms in these disorders, but available empirical evidence remains scarce. Developing and testing a theoretical model of the co-occurrence between PDs and sleep difficulties could be the target of future research. Such model might help in developing an integrated treatment. Future studies should also examine the unique relation between insomnia and
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other DSM-5 personality disorders. These studies may further highlight the need for clinicians to adapt their treatment approach with these patients. In the short
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term, we recommend that clinicians screen for the presence of sleep problems when evaluating patients with a PD and consider the possibility of treating
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insomnia. Conversely, maladaptive personality traits could be assessed before
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treating insomnia.
Finally, researchers should also document the use of medication or other substances which might interfere with treatment efficacy or potentiate sleep
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problems in any mental disorder (e.g. worsening sleep). This area is often overlooked in current research, especially when substance abuse disorders are
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present.
2. Substance use disorder (SUD) 2.1. Comorbidity between SUD and insomnia. Systematic and narrative literature reviews indicate that the use of substances and sleep disorders share a
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bidirectional relationship [27-29]. Insomnia can be present before substance dependence or abuse, or be associated with withdrawal (lasting for weeks) and relapse [27]. In their literature review, Grau-López et al. [30] reported that in studies recruiting patients with a SUD, the prevalence of insomnia ranges from 30% to 85% depending on the primary substance of abuse. Conversely, Dolsen et al. [31](*) found that individuals with a lifetime history of insomnia symptoms
used substances (i.e. alcohol, cocaine, and heroin) more frequently than good sleepers. 2.2. Substance use as a risk factor for sleep impairments. Chronic substance use severely affects the duration and quality of sleep, and these deleterious effects can also be observed during withdrawal [32]. Indeed, although the effect is dose-dependent, most drugs impact the amount of time spent in the different stages of sleep or the timing of NREM and REM sleep cycles, as well as both the
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subjective and objective quality and quantity of sleep [32-35]. In a review by
Chakravorty et al. [33](*), the most frequent sleep-related complaints in patients
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with SUD (i.e. alcohol, opioids, cannabis, cocaine, or sedative-hypnotic-anxiolytic drugs) included increased sleep latency and time awake after sleep onset.
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Recent studies have analyzed the effect of specific drugs, benzodiazepines (BZD) and opioids, on sleep. In one study [36], the long-term use of high doses
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of BZD for the treatment of chronic insomnia decreased slow wave brain activity. Regarding the effects of opioids, a single dose can improve subjective sleep
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quality in patients with chronic pain and insomnia [33], while it significantly alters sleep architecture in healthy adults [27]. Angarita et al. [27] reported that chronic or long-term use of opioids may lead to self-reported sleep dysfunction such as
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increased sleep latency, increased awakening, decreased total sleep time, and decreased sleep efficiency.
2.3. Insomnia as a risk factor for substance abuse. Drugs or alcohol can be used as self-medication attempts to facilitate sleep or to reduce the physical and
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emotional burden resulting from sleep difficulties [31,37]. In a sample of individuals with insomnia, the severity of insomnia was related to a higher likelihood of using cocaine at 12-months post-treatment, possibly as an attempt to alleviate a withdrawal-induced rebound in insomnia [31]. Furthermore, in a placebo controlled experiment, Roehrs and Roth [29] have shown that individuals with insomnia are at higher risk of substance abuse if they exhibit autonomic (i.e. elevated daytime urinary norepinephrine levels) or behavioral signs of
hyperarousal (i.e. higher nap sleep latency). From a clinical standpoint, this result suggests that reducing daytime hyperarousal in individuals with insomnia may prevent self-medication attempts. 2.4. Insomnia during withdrawal. While the effects of chronic long-term use of various drugs and substances on sleep have been investigated, withdrawal symptoms may have been neglected. In a review [38] on the effects of cannabis withdrawal on sleep, when abstaining from cannabis use, at least one third of
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participants reported experiencing trouble sleeping, strange dreams and waking up early, as well as a self-reported reduction insleep duration. Furthermore,
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sedative-hypnotic-anxiolytic drugs (including BZD and non-BZD) are often
prescribed to facilitate sleep [33]. However, abrupt cessation of these drugs,
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especially BZD, has been associated with sleep complaints such as decreased total sleep time and a poor sleep quality [33]. Indeed, attempting to quit
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sedative-hypnotic-anxiolytic drugs such as BZD may result in “rebound insomnia” (i.e. exacerbation of sleep disturbances) that may be even worse than before the use of the medication [39]. Encouragingly, studies found that intensive
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psychosocial support [40] or Cognitive Behavioral Therapy for Insomnia (CBT-I) [41] may markedly improve sleep and quality of life in older adults with primary
drugs.
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insomnia during withdrawal from long‐term use of sedative-hypnotic-anxiolytic
2.5. SUD and insomnia: clinical implications and future directions. There is strong evidence supporting the bidirectional relationship between SUD and insomnia [42]. While substance use is known to impact sleep, notwithstanding
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the substance, insomnia symptoms seem to contribute to the development and maintenance of SUD. Furthermore, there is growing but limited evidence on the effectiveness of insomnia treatment in patients with SUD [41,43,44]. In individuals with insomnia comorbid with another psychiatric condition (e.g., SUD), objective and subjective sleep quality can be fostered with CBT-I beyond the effect of pharmacotherapy [41,45]. Notably, CBT-I may include an optional module for discontinuing hypnotic medications [41], the tapering being
supervised by a physician. Thus, another area of research would be to examinetreatments that specifically target sleep disturbances in the context of withdrawal in individuals with a SUD. From a clinical perspective, when working with patients who present a SUD and insomnia, clinicians should be aware that these conditions are both linked to suicidality. Indeed, substance use (except LSD and psychedelic drugs [46]) is linked to suicidal ideation and attempts [47], as is insomnia [48]. More
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precisely, the risk of suicide is almost 18 times higher in insomnia than in non-insomnia populations [49]. Still, very few studies have tied insomnia,
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substance abuse, and suicide risk in the same predictive model [50]. Thus, future research may assess the possible additivity in the risk of suicide in individuals
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who present a SUD and insomnia compared to those who only present one of these disorders. Moreover, researchers have suggested that we identify
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individuals with a SUD who are at-risk for future relapse and who present comorbid sleep complaints to better inform prevention and intervention efforts, in
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the hope of also reducing the risk of suicide [37]. Conclusion
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Only a paucity of research exists in the field of personality disorders and insomnia. The relationship between substance use disorder and insomnia, on the other hand, has received more attention. Although the study of objective sleep is not recommended for the diagnosis of insomnia, this approach has highlighted peculiarities in the sleep of individuals with a PD or a SUD. For instance,
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individuals with a BPD present increased sleep onset latency and lower sleep efficiency. Importantly, emotion dysregulation appears to promote a mutually aggravating relationship between insomnia and BPD. In individuals with a SUD, insomnia can be present during periods of substance abuse and/or during withdrawal. Moreover, insomnia can increase the risk of relapse. This review highlights that insomnia is part of many personality disorders and substance use disorders in addition to be linked to suicidal ideation. Thus, from a transdiagnostic perspective, targeting insomnia during treatment can be a
promising avenue to increase the general well-being of individuals presenting these psychological difficulties. Randomized control studies targeting comorbid PDs and SUD in association with insomnia are needed to document the contribution of these respective disorders on sleep difficulties and vice-versa. Alternatively, taking a precision medicine approach could be ideal since the clinical picture of comorbid disorders is often complex. Dissemination of treatment efficacy and how to maintain therapeutic gains would be beneficial for
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all.
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None of the authors have any conflict of interests.
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