Final Report Summary - EMOTIONS IN INSOMNIA (The neurobiological bases of emotion processing in Primary Insomnia)
Heightened subjective emotional reactivity is considered as a maintaining factor for insomnia (for a review see Baglioni et al., 2010a). Studies conducted through subjective self-report measures (e.g. Scott and Judge, 2006; McCrae et al., 2008) are consistent in finding an increased response to negative emotional stimuli in insomnia. Moreover, insomnia leads to an increased risk of affective disorders (Baglioni et al., 2011). However the role of the physiological correlates of emotional processes in insomnia has been rarely investigated (e.g. Baglioni et al., 2010b).
The aim of this study was to evaluate the role of emotional reactivity in primary insomnia, based on a multidisciplinary approach using the combination of psychological and neuroimaging methods. Twenty-two patients with primary insomnia and forty healthy good sleepers took part in the study. Each participant underwent: 1) a clinical interview in order to rule out any psychiatric disorder; 2) 2 consecutive nights of polysomnographic recordings (an adaptation night and a baseline night) in order to rule out any other sleep disorder different from insomnia; 3) an fMRI emotional task. Additionally, each participant filled out a list of questionnaires evaluating sleep, emotions and psychiatric characteristics.
The fMRI emotional task consisted in one-session lasting for 13 minutes and 20 seconds. Stimuli were selected based on valence and arousal dimensions and were classified in 5 content-specific blocks: low arousal neutral pictures; high arousal negative pictures; matched arousal neutral, negative and sleep-related negative pictures. In order to check for attention to the task, a recognition task was conducted at the end of the session. In order to control for sleepiness and anxiety, before the beginning of the fMRI session all participants filled out the Stanford Sleepiness Scale (SSS, Hoddes et al., 1973) and the state version of the State Trait Anxiety Scale (STAI, Spielberger et al., 1970).
Considering all the 22 patients with insomnia and 40 healthy controls, the groups differed in sleep quality on the baseline night: specifically, patients with insomnia presented decreased total sleep time, sleep efficiency, and REM sleep percentage. Additionally, patients with insomnia presented impairment in all sleep questionnaires as compared to healthy controls. The groups did not differ for depression as measured through the Beck Depression Inventory (BDI, Beck et al., 1961), while people with insomnia reported higher scores in the trait version of the State Trait Anxiety Inventory (STAI), however the means for both groups did not reach the cut off considered for possible clinical anxiety (cut-off=40). Groups were not different for level of sleepiness and state anxiety before the fMRI sessions. In the recognition task, people with insomnia performed worst as compared to the healthy controls.
Preliminary results conducted on 15 patients with primary insomnia and 40 controls showed that all participants taken together responded with higher activation of the amygdala and other brain areas connected (e.g. middle occipital gyrus) to the view of high arousal negative stimuli as compared to low arousal negative stimuli (see Figure 1 attached). When analysing group differences, we found that patients with insomnia presented a less intense response in all these areas as compared to healthy controls.
With respect to the sleep-related negative stimuli, all participants taken together responded with higher activation of brain areas involved in the vision of emotional visual stimuli and/or in the vision of faces (e.g. temporal gyrus, cuneus). When analysing group differences, however, we did not find any statistical significant difference between the groups.
It could be possible that individuals with insomnia respond with increased levels of arousal to low arousal neutral stimuli compared to healthy controls. Thus, the difference between the intensity of the response to high arousal negative stimuli and low arousal neutral stimuli would be not as marked in the patient-group compared to the control-group. Although preliminary, these results might suggest that primary insomnia is a condition specifically linked to high levels of arousal. The chronic aspect of the disorder would lead to a worsening of the quality of life which is initially linked to a deterioration of the emotional subjective experience. In the long-term the relationships between poor sleep and reduced quality of life/subjective experience of emotions would lead to an impairment of the emotional system leading to an increase risk for affective psychiatric disorders. Another explanation could focus on REM sleep. People with insomnia present a reduced amount of REM sleep as compared to healthy controls (Feige et al., 2008); instead major depression is characterized by an increase of REM sleep. It could be hypothesized that as the disorder gets chronic, it increases the risk for a REM sleep rebound which would lead to periods rich of REM sleep, and consequently facilitate the development of a depressive episode.
SOCIO-ECONOMIC IMPACT. The following results suggests that there is a long-term causal sequence between insomnia and depression in which high levels of hyperarousal would interfere with the emotional system up to leading to its alteration and to depressive symptoms. Recently it has been proposed that this sequence is not specific only for depression, but for psychopathology in general (Harvey et al., 2011). Consequently, treating sleep difficulties at an early stage could prevent affective consequences. However, up to now, treatment for chronic insomnia is either not effective in long term (hypnotic medications) or effective in long term but not available to most of the patients (psychological cognitive-behaviour treatment of insomnia). "Stepped care models" and internet interventions have been tested preliminarily in insomnia with positive results. Knowledge on and interventions for insomnia should be widespread in the general population in order to treat it at its early manifestations, blocking a possible worsening of the condition and the development of other psychiatric disorders. Additionally to that, as insomnia is a widespread condition in all main psychiatric disorders, treatment of insomnia should be implemented and diffused in primary care.
REFERENCES. 1) Baglioni et al. (2010a). Sleep Medicine Reviews, 14(4): 227-38; 2) Baglioni et al. (2011). Journal of Affective Disorders, 2011, in press; 3) Baglioni et al. (2010b). Behaviour Research and Therapy, 48(6): 467-75; 4) Hoddes et al. (1973). Psychophysiology, 10(4): 431-6; 5) Spielberger et al. (1970). Palo Alto, Calif: Consulting Psychologist Press; 6) Beck et al. (1961). Archives of General Psychiatry, 4: 561-71; 7) Harvey et al. (2011). Clinical Psychology Reviews, 31: 225-35; 8) Feige et al. (2008). Journal of Sleep Research, 17(2): 180-90.
The aim of this study was to evaluate the role of emotional reactivity in primary insomnia, based on a multidisciplinary approach using the combination of psychological and neuroimaging methods. Twenty-two patients with primary insomnia and forty healthy good sleepers took part in the study. Each participant underwent: 1) a clinical interview in order to rule out any psychiatric disorder; 2) 2 consecutive nights of polysomnographic recordings (an adaptation night and a baseline night) in order to rule out any other sleep disorder different from insomnia; 3) an fMRI emotional task. Additionally, each participant filled out a list of questionnaires evaluating sleep, emotions and psychiatric characteristics.
The fMRI emotional task consisted in one-session lasting for 13 minutes and 20 seconds. Stimuli were selected based on valence and arousal dimensions and were classified in 5 content-specific blocks: low arousal neutral pictures; high arousal negative pictures; matched arousal neutral, negative and sleep-related negative pictures. In order to check for attention to the task, a recognition task was conducted at the end of the session. In order to control for sleepiness and anxiety, before the beginning of the fMRI session all participants filled out the Stanford Sleepiness Scale (SSS, Hoddes et al., 1973) and the state version of the State Trait Anxiety Scale (STAI, Spielberger et al., 1970).
Considering all the 22 patients with insomnia and 40 healthy controls, the groups differed in sleep quality on the baseline night: specifically, patients with insomnia presented decreased total sleep time, sleep efficiency, and REM sleep percentage. Additionally, patients with insomnia presented impairment in all sleep questionnaires as compared to healthy controls. The groups did not differ for depression as measured through the Beck Depression Inventory (BDI, Beck et al., 1961), while people with insomnia reported higher scores in the trait version of the State Trait Anxiety Inventory (STAI), however the means for both groups did not reach the cut off considered for possible clinical anxiety (cut-off=40). Groups were not different for level of sleepiness and state anxiety before the fMRI sessions. In the recognition task, people with insomnia performed worst as compared to the healthy controls.
Preliminary results conducted on 15 patients with primary insomnia and 40 controls showed that all participants taken together responded with higher activation of the amygdala and other brain areas connected (e.g. middle occipital gyrus) to the view of high arousal negative stimuli as compared to low arousal negative stimuli (see Figure 1 attached). When analysing group differences, we found that patients with insomnia presented a less intense response in all these areas as compared to healthy controls.
With respect to the sleep-related negative stimuli, all participants taken together responded with higher activation of brain areas involved in the vision of emotional visual stimuli and/or in the vision of faces (e.g. temporal gyrus, cuneus). When analysing group differences, however, we did not find any statistical significant difference between the groups.
It could be possible that individuals with insomnia respond with increased levels of arousal to low arousal neutral stimuli compared to healthy controls. Thus, the difference between the intensity of the response to high arousal negative stimuli and low arousal neutral stimuli would be not as marked in the patient-group compared to the control-group. Although preliminary, these results might suggest that primary insomnia is a condition specifically linked to high levels of arousal. The chronic aspect of the disorder would lead to a worsening of the quality of life which is initially linked to a deterioration of the emotional subjective experience. In the long-term the relationships between poor sleep and reduced quality of life/subjective experience of emotions would lead to an impairment of the emotional system leading to an increase risk for affective psychiatric disorders. Another explanation could focus on REM sleep. People with insomnia present a reduced amount of REM sleep as compared to healthy controls (Feige et al., 2008); instead major depression is characterized by an increase of REM sleep. It could be hypothesized that as the disorder gets chronic, it increases the risk for a REM sleep rebound which would lead to periods rich of REM sleep, and consequently facilitate the development of a depressive episode.
SOCIO-ECONOMIC IMPACT. The following results suggests that there is a long-term causal sequence between insomnia and depression in which high levels of hyperarousal would interfere with the emotional system up to leading to its alteration and to depressive symptoms. Recently it has been proposed that this sequence is not specific only for depression, but for psychopathology in general (Harvey et al., 2011). Consequently, treating sleep difficulties at an early stage could prevent affective consequences. However, up to now, treatment for chronic insomnia is either not effective in long term (hypnotic medications) or effective in long term but not available to most of the patients (psychological cognitive-behaviour treatment of insomnia). "Stepped care models" and internet interventions have been tested preliminarily in insomnia with positive results. Knowledge on and interventions for insomnia should be widespread in the general population in order to treat it at its early manifestations, blocking a possible worsening of the condition and the development of other psychiatric disorders. Additionally to that, as insomnia is a widespread condition in all main psychiatric disorders, treatment of insomnia should be implemented and diffused in primary care.
REFERENCES. 1) Baglioni et al. (2010a). Sleep Medicine Reviews, 14(4): 227-38; 2) Baglioni et al. (2011). Journal of Affective Disorders, 2011, in press; 3) Baglioni et al. (2010b). Behaviour Research and Therapy, 48(6): 467-75; 4) Hoddes et al. (1973). Psychophysiology, 10(4): 431-6; 5) Spielberger et al. (1970). Palo Alto, Calif: Consulting Psychologist Press; 6) Beck et al. (1961). Archives of General Psychiatry, 4: 561-71; 7) Harvey et al. (2011). Clinical Psychology Reviews, 31: 225-35; 8) Feige et al. (2008). Journal of Sleep Research, 17(2): 180-90.