The Effect of Depersonalization and Derealization Symptoms

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THE EFFECT OF DEPERSONALIZATION AND DEREALIZATION SYMPTOMS

ON OLFACTION AND OLFACTORY HEDONICS

Thesis

Submitted to

The College of Arts and Sciences of the

UNIVERSITY OF DAYTON

In Partial Fulfillment of the Requirements for

The Degree of

Master of Arts in Psychology

Rhiannon A. Gibbs

UNIVERSITY OF DAYTON

Dayton, Ohio

May 2018

THE EFFECT OF DEPERSONALIZATION AND DEREALIZATION SYMPTOMS

ON OLFACTION AND OLFACTORY HEDONICS

Name: Gibbs, Rhiannon A.

APPROVED BY:

______Julie Walsh-Messinger, Ph.D. Faculty Advisor

______Roger R. Reeb, Ph.D. Committee Member

______Jackson A. Goodnight, Ph.D. Committee Member

Concurrence:

______Lee Dixon, Ph.D. Chair, Department of Psychology

Rhiannon A. Gibbs

2018

ABSTRACT

THE EFFECT OF DEPERSONALIZATION AND DEREALIZATION SYMPTOMS

ON OLFACTION AND OLFACTORY HEDONICS

Name: Gibbs, Rhiannon A. University of Dayton

Advisor: Dr. Julie Walsh-Messinger.

Depersonalization and derealization symptoms affect sensation, perception, and emotion, producing subjective experiences of unreality and affective numbing (Simeon, 2004).

Abnormalities in the amygdala, which is associated with emotional reactions such as anxiety and fear (LeDoux, 1993), have been observed in depersonalization and derealization and other psychiatric disorders, such as anxiety and depression (Sierra &

Berrios, 1998). Olfactory deficits have been posited as a potential marker for psychiatric disorders, including depression (Atanasova, 2008), which may be related to the close neural connections between the olfaction system and the amygdala (Stockhorst &

Pietrowsky, 2004). However, no previous studies have examined the relationship between depersonalization/derealization and olfactory functioning. Thus, this study investigated whether depersonalization and derealization symptom severity was correlated with odor identification ability, odor detection threshold, and hedonic ratings of odors in an undergraduate sample (N = 92). It was hypothesized that: 1) odor

iii identification ability would be negatively correlated with reported depersonalization and derealization symptoms; 2) odor detection threshold would be positively correlated with depersonalization and derealization symptoms; and 3) both pleasantness and unpleasantness ratings of odors would be negatively correlated with depersonalization and derealization symptoms. Participants (N = 92) were administered two olfaction testing batteries, and completed self-report measures of depersonalization, depression, and anxiety. Results did not support the main hypotheses. Exploratory analyses revealed a significant sex by depersonalization interaction for odor identification ability, indicating that females with higher levels of depersonalization were less able to correctly identify odorants. Future research in clinical samples is needed to confirm this interaction.

iv ACKNOWLEDGEMENTS

First of all, I would like to thank my incredible advisor, Dr. Julie Walsh-

Messinger, for her unwavering support and guidance. Her sound advice, and at times constructive criticisms, were invaluable to the development of this project. I could not have imagined a better mentor to work with and extend to her my deepest gratitude.

Secondly, I would like to thank the members of my committee, Dr. Roger Reeb and Dr. Jackson Goodnight, for their insight, encouragement, and difficult questions.

Their input was extraordinarily helpful in the development of this study.

I would also like to thank Russell Mach, Julia Weideman, Lisa Stone, Lauren

Olson, Maia Mclin, and all other current and former members of the Personality and

Smell lab, for their assistance in collecting and entering data. Their hard work made this study possible.

Finally, I would like to thank my wonderful family, friends, and fellow classmates at the University of Dayton. Their love, friendship, and support have been unfailing for the last two and a half years, and this project could not have happened without it. Thank you.

v TABLE OF CONTENTS

ABSTRACT……………………………………………………………………………...iii

ACKNOWLEDGMENTS………………………………………………………………...v

LIST OF TABLES………………………………………………...... vii

INTRODUCTION………………………………………………………………………...1

METHODS...…………………………………………………………………………….16

RESULTS………………………………………………………………………………..20

DISCUSSION……………………………………………………………………………29

REFERENCES…………………………………………………………………………..35

APPENDICES

A. Cambridge Depersonalization Scale….…………………………………...….42

B. Generalized Anxiety Disorder 7 Item Scale…….………………………….....44

C. Center for Epidemiologic Studies Depression Scale Revised ……………...... 45

D. Odor Hedonic Rating Scales…………..……………………………………...47

vi LIST OF TABLES

Table 1. Means and Standard Deviations for All Measures……………………………20

Table 2. Tests of Normality…………………………………………………………….21

Table 3. Correlation Table……………………………………………………………...21

Table 4. Results of Multiple Regression Analyses- Odor Identification……………….22

Table 5. Results of Multiple Regression Analyses-Threshold Detection………………22

Table 6. Results of Multiple Regression Analyses- Unpleasantness and Pleasantness Ratings…………………………………………………………………………………...23

Table 7. Means and Standard Deviations for all Measures, by Sex……………………24

Table 8. Independent Samples T-Tests for all Measures, by Sex………………………24

Table 9. Results of Multiple Regression Analyses in Males- Odor Identification……..24

Table 10. Results of Multiple Regression Analyses- Females…………………………..25

Table 11. Results of Multiple Regression Analyses in Males- Threshold Detection……25

Table 12. Results of Multiple Regression Analyses in Females- Threshold Detection….25

Table 13. Results of Multiple Regression Analyses in Males- Unpleasantness and Pleasantness Ratings……………………………………………………………………..26

Table 14. Results of Multiple Regression Analyses in Females- Unpleasantness and Pleasantness……………………………………………………………………………...26

Table 15. Mean Differences for Sex x Depersonalization Group Interaction…………...27

vii

CHAPTER 1

INTRODUCTION

Depersonalization is a perceptual anomaly characterized by subjective feelings of unreality and alterations in the perception of the self. This sensation involves feelings of detachment from oneself, alterations in the perception of one’s identity, and/or emotional numbing (APA, 2013). Common descriptions include feeling numb, robotic, unreal, or as though one’s body is foreign. Derealization, by contrast, is characterized by subjective feelings of unreality and/or detachment in relation to external surroundings. Common descriptions include feeling as though the world is hazy, foggy, dreamlike, or like there is a pane of glass in front of one’s eyes (Simeon, 2004).

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-

5) classifies depersonalization/derealization disorder (DDD) as a dissociative disorder characterized by chronic and/or recurring symptoms of depersonalization and/or derealization. No operational time limit for frequency and duration of symptoms is specified, but transient symptoms generally are not indicative of a disorder. Symptoms must also cause clinically significant distress and/or impairment in functioning, and reality testing must remain intact. Symptoms must not be better accounted for by another mental disorder (such as panic disorder, posttraumatic stress disorder, or another dissociative disorder,) and must not be caused by a general medical condition or drug and

alcohol use (APA, 2013).

Prevalence rate estimates of DDD range from 0.8 to 2.8 percent in the general population (APA, 2013). In non-clinical populations, the lifetime prevalence of subclinical, transient depersonalization symptoms is estimated at between 26 and 74 percent (Hunter, Sierra, & David, 2004). DSM-5 estimates the lifetime prevalence of subclinical symptoms to be roughly 50 percent in the general population (APA, 2013). As well, Aderibigbe, Bloch, and Waler (2001) found annual prevalence rates for depersonalization experiences in a rural population to be roughly 23 percent. These experiences were categorized as non-clinical because participants were asked only if they had experienced depersonalization symptoms for at least one hour, or at least 3 times in the past year (Aderibigbe et al., 2001). Simeon (2004) suggests that depersonalization and derealization symptoms are more common in the general population than is often believed by the psychiatric community. It is probable that symptoms are frequently mistaken as variations of depression and anxiety (Simeon, 2004).

Clinical features of depersonalization and derealization are based on subjective experiences of unreality, and remain difficult to define and identify by clinicians. One study presented findings from 204 cases of DDD and identified several clinical features of the disorder, including the tendency to be chronic, highly co-morbid with depression and anxiety, and associated with trauma, non-traumatic psychological stressors, and substance misuse (Baker et al., 2003). Other studies have also identified high prevalence of depersonalization/derealization symptoms among those with panic disorder, unipolar depression, and posttraumatic stress disorder (Hunter et al., 2004,) and high co- morbidities of DDD with mood, anxiety, and personality disorders (Simeon, Knutelska,

Nelson & Guralnik, 2001). Given these frequently observed co-morbidities, it is possible that the neurological mechanisms of these disorders overlap.

Along with perceptual anomalies, sensory abnormalities are common experiences in depersonalization and derealization. People with DDD often describe the world as seemingly two-dimensional, flat, or colorless (Radovic & Radovic, 2003), and report a sensation of disconnection and numbness from bodily stimuli (Simeon, 2004). At the same time, people with DDD report a hyper-awareness of bodily sensations that may contribute to the alien and unreal feelings associated with the disorder (Sierra & Berrios,

1998).

Depersonalization/derealization, and dissociative symptoms in general, have historically been conceptualized as defense mechanisms, which are unconscious coping responses to trauma that may be linked to personality factors (Kihlstrom, Glisky, &

Angiulo, 1994). In psychodynamic theory, defense mechanisms typically develop as a coping mechanism for trauma and may exist to help defend the individual against further perceived threats, be they internal or external. In particular, depersonalization may defend from being able to subjectively experience the full impact of trauma (Shilony &

Grossman, 1993). This psychodynamic conceptualization dates back to the early 20th century. Sigmund Freud was reported to have experienced an episode of depersonalization while visiting the Acropolis in Greece, and as such considered the experience a defense against external stimuli that were too overwhelming or difficult to process (Feigenbaum, 1937).

Other psychodynamic explanations for depersonalization describe it as a disease of the ego, in which a lack of libidinal drive effected the ‘structural core’ and

‘boundaries’ of the ego (Federn, 1953). Another psychoanalyst, Oberndorf (1934) believed the opposite, that depersonalization was a result of an increase in libidinal investment. Fenichel (1945) clarified that depersonalization acted as a defense mechanism guarding against libidinal drives, which are unpleasant to the ego. One of the more common themes of psychoanalytic explanations is that depersonalization serves as a defense against ‘anxiogenic intrapsychic conflict’ (Oberndorf, 1950).

As a term, depersonalization was first coined by Ludovic Dugas in 1898, while studying associations with false memories. Dugas would later describe depersonalization as being the result of a failure of integration of information caused by apathy. Apathy, in this sense, referred to an elimination of emotional processing, and was described as the sense of the loss of personhood in the patient (Dugas, 1898). Earlier descriptions of symptoms believed to be consistent with the modern definition of depersonalization were often described in relation to symptoms associated with melancholia, or depression

(Sierra & Berrios, 1997).

Other early conceptualizations focused on sensory impairment resulting from pathological changes in the body (Sierra & Berrios, 1997). The earliest sensory explanations for depersonalization were described as being caused by a pathology of the sensory system (Krishaber, 1873). Neurological explanations were believed by many to be the primary precipitating factor of depersonalization symptoms (Sierra & Berrios,

1997). Foerster (1903), a student of Carl Wernicke, suggested depersonalization was a result of unsynchronized sensory and muscular systems in the brain, which led to the perceived disconnection between self and body. Wernicke himself thought depersonalization resulted from a distorted bodily awareness which stemmed from

abnormalities in the proprioceptive system (Wernicke, 1906). These sensory explanations were later challenged by psychodynamic models (Sierra & Berrios, 1997).

Empirical support for early psychodynamic theories exists only in that depersonalization may act as a defense mechanism similar to other forms of dissociation

(Shilony & Grossman, 1993). Historical conceptualizations, however, have influenced the current conceptualization of depersonalization as a dissociative disorder (Sierra &

Berrios, 1997). Additionally, the sensory functioning and neurobiological underpinnings of depersonalization remain a major focus for current depersonalization research.

Neurobiology

Sierra and Berrios (1998) theorized the deep limbic system (in particular the amygdala), anterior cingulate, and prefrontal cortex, to be neural structures underlying

DDD. They conceptualized depersonalization and derealization as a response to extreme anxiety, in which the left prefrontal cortex produces an inhibitory response upon the amygdala and other deep limbic structures, contributing to the subjective feelings of unreality and hypoemotionality characteristic of depersonalization. This does appear to line up with the subjective phenomenology of depersonalization, such as feeling “numb” or “robotic,” and experiencing a sense of detachment from emotional processing.

Sierra and Berrios (1998) then posited that in response to limbic inhibition, the amygdala indirectly influences the anterior cingulate, while simultaneously producing an excitatory response on the ascending arousal systems and right prefrontal cortex. This excitatory component to depersonalization/derealization may explain the hyperarousal that tends to occur (i.e., obsessive rumination over symptoms, hypervigilance.) The authors suggested that this system is meant to be an adaptive threat response, and DDD

occurs when this system is continually active in nonthreatening contexts. This theory is consistent with the historical conceptualization of DDD as a defense mechanism, given that defense mechanisms are conceptualized as a response to threatening stimuli.

This theory is further supported by evidence which illuminates the role of the amygdala and other limbic structures in the processing of emotions and consolidation of emotional memory. According to LeDoux (1993), the amygdala is highly involved in the processing of emotional memory. This process can be mediated by sensory input from both the thalamus and cerebral cortex. These sensory cues play a role in creating associations with emotional memories and in memory consolidation (LeDoux, 1993).

Moreover, emotional memory consolidation appears linked to hippocampal functioning as well as the amygdala. While the hippocampus and amygdala typically function within independent memory systems, they can interact. The amygdala can modulate the processing of memory in the hippocampus, enhancing the emotional salience of memories, which tend to be stronger than less emotional memories (Cahill &

Alkire, 2003, Cahill, Gorski, & Le, 2003). As well, episodic hippocampal memories can influence the amygdala when activated, producing strong emotional responses. The relationship appears bi-directional (Richardson, Strange, & Dolan, 2004).

Research on brain glucose activity posited potential associations between cerebral activity and depersonalization symptoms. Simeon et al. (2000) used positron emission tomography (PET) scans to compare the brain glucose metabolism of individuals with

DDD to healthy controls. In the DDD group, glucose hypoactivity was found within the right superior and middle temporal gyri (Brodmann’s areas 22 and 21), which are both implicated in the processing and generating of language. Area 22 is also implicated in

processing pitch and intensity of sound in the right hemisphere. Glucose hyperactivity was observed in the right parietal lobe (Brodmann’s areas 7B and 39), which is responsible for somatosensory and spatial processing, and integration of somatosensory, visual, and auditory stimuli. Finally, hyperactivity was also found in the left occipital lobe (Brodmann’s area 19), which is responsible for the visual integration of shapes

(Simeon et al., 2000). Hyperactivity and hypoactivity in sensory and perceptual areas of the brain may, in part, explain the characteristic disturbances in perception observed in depersonalization/derealization symptoms (Simeon et al., 2000).

More current research examining the relationship between brain functioning and

DDD suggested that people with DDD showed significantly lower activation of brain areas associated with emotional processing when presented with an emotional word encoding task (Medford, Brierly, Brammer, David, & Phillips, 2006). Brain areas associated with emotional processing were observed via functional magnetic resonance imaging (fMRI), and included the hippocampus, amygdaloid complex, and anterior cingulate. Participants with DDD showed no differences in their neural responses to neutral words versus emotional words in these regions, as well as showing lower activation during the emotional word encoding task. Medford et al. (2006) suggested this is evidence that in DDD, emotional stimuli are processed in different ways, more similar to the processing of neutral stimuli. This is posited to be one theoretical explanation for the reported emotional numbing frequently associated with DDD (Medford et al., 2006).

In another fMRI study, findings showed that when compared to participants with obsessive compulsive disorder (OCD) and healthy controls, participants with DDD experienced less activation in brain regions associated with disgust and emotional

processing (the insula; occipito-temporal cortex), when presented with aversive stimuli

(Phillips et al., 2001). Instead, the aversive stimuli activated the right ventral prefrontal cortex, an area thought to play a role in inhibition. Neutral stimuli actually triggered greater neural activation in participants with DDD than the control groups, notably in the left insula (Phillips et al., 2001). This suggests some degree of abnormality of emotional processing in people with DDD, and that the insula may play a role.

Mula, Pini, and Cassano (2007) noted that Sierra and Berrios (1998)’s theory, as well as other findings related to limbic functioning, have not adequately accounted for somatosensory symptoms of depersonalization/derealization. Mula et al. (2007) posited that the findings of Simeon et al. (2000) suggest that the somatosensory symptoms of depersonalization and derealization may still be connected to abnormalities originating in the amygdala and deep limbic system, by acting on sensory and perceptual processing areas of the cerebral cortex. The cerebral cortex may be responding to messages received from the limbic system and behaving accordingly. However, the exact mechanism by which DDD operates is not currently known, and these theories are only speculative.

Cognition

DDD appears to have significant effects on cognitive processes related to perception, attention, and memory. For example, one study found that 71% of participants with DDD had self-reported impairments in memory and concentration

(Baker et al., 2007). Guralnik, Schmeidler, and Simeon (2000) found that participants with DDD scored significantly lower on tests of visual memory, logical associations, and ability to remember visual pairs, as measured by the Wechsler Memory Scale, Revised

(WMS-R; Wechsler, 1997). Of note, overall memory was also significantly lower for the

DDD group. As well, individuals with DDD scored significantly lower on Block Design, a visual-motor and non-verbal reasoning subtest of the Wechsler Adult Intelligence Scale,

Revised (WAIS-R; Wechsler, 1981), but had comparable Full-Scale Intelligence Quotient scores (Guralnik et al., 2000). These findings suggested that while DDD does not cause global impairments, such as those found in schizophrenia or other psychotic disorders, it does contribute to certain impairments in visual and perceptual functioning consistent with subjective symptom complaints (Guralnik et al., 2000). Whether these impairments are caused by DDD or contribute to the development of DDD is unclear at this time, given the correlational nature of these research studies.

A study using a facial recognition task found that individuals with DDD performed significantly worse for recognition of anger compared to healthy controls

(Montagne et al., 2007). This is consistent with Sierra and Berrios (1998)’s theory that depersonalization and derealization symptoms are meant to nullify perception of threatening stimuli. DDD then develops when symptoms persist even when threats are not present, perhaps as a defect in a naturally occurring system of defense (Montagne et al., 2007). A different facial recognition study using fMRI found that participants with

DDD showed decreases in sub-cortical activity, particularly the hypothalamus and amygdala, in response to increasingly happy or sad facial expressions (Lemche et al.,

2007). These findings notably aligned well with the neurobiological theory proposed by

Sierra and Berrios (1998) by confirming that sub-cortical inhibition is implicated in

DDD.

Olfaction

Given that abnormalities have been identified in visual, auditory, and somatosensory brain regions in people with DDD, it would stand to reason that other sensory abnormalities may be involved in the disorder. While visual, auditory, and tactile systems have larger bodies of research, the chemical senses of olfaction and gustation remain an important component of human sensory and perceptive systems. Olfaction, in particular, plays a large role in emotional processing, memory, and social behaviors

(Stockhorst & Pietrowsky, 2004), all of which may be abnormal in individuals with DDD

(Simeon, 2004).

The olfactory system is comprised of at least four different neural systems: the main olfactory system, the trigeminal system, the accessory olfactory system, and the terminal nerve (Stockhorst & Pietrowsky, 2004). The main olfactory system is responsible for the perception of vaporizable chemicals, while the trigeminal system perceives pungent, cold, or burning odors. The functions of the accessory and terminal systems are less clear, but may be involved in the detection of pheromones and their impact on reproductive behavior (such as mate seeking and selection) based on studies in non-human animals. The accessory system also includes the vomeronasal organ, which evidence suggests is sexually dimorphic (Stockhorst & Pietrowsky, 2004). Olfaction begins in the nasal passages, where receptor cells make up the olfactory epithelium in the nasal mucosa. From there, action potentials are sent to the olfactory bulb, located at the base of the forebrain. These signals then project directly to the primary olfactory cortex

(Stockhorst & Pietrowsky, 2004).

Unlike most senses, olfactory signals bypass the thalamus, or relay center of the brain, and are instead projected directly to the olfactory cortex, which is comprised of the anterior olfactory nucleus, prepiriform cortex, lateral entorhinal cortex, olfactory tubercle, and cortical nucleus of the amygdala (Stockhorst & Pietrowsky, 2004). Signals from the olfactory cortex then project to sub-cortical structures including the hypothalamus, medial thalamus, hippocampus, as well as the substantia innominata, septal region, mesencephalic reticular system, and orbitofrontal cortex (Stockhorst &

Pietrowsky, 2004).

Due to this close association with the limbic system, it is thought that the emotional (hedonic) component of olfaction tends to be greater than that of other sensory systems (Stockhorst & Pietrowsky, 2004). A study of healthy older adults found that memories evoked by olfactory stimuli produced higher emotional arousal than did memories evoked by verbal cues, tended to be older, were rated as more pleasant, and induced a greater sense of immersion in time (Willander & Larsson, 2007). The authors suggested that odor-induced memories may be operating differently than other varieties of memory retrieval. Greater emotional memory recognition and episodic retrieval of experimental conditions were shown to be associated with odors rated as both pleasant and unpleasant compared to neutral odors, suggesting the emotional intensity of odor is implicated in the retrieval of memories associated with the odor (Saive et al., 2014).

These findings are consistent with the close neurobiological link between olfaction and emotion processing centers of the brain (Stockhorst & Pietrowsky, 2004).

As such, abnormalities in hedonic ratings of odors may be a marker for abnormal limbic functioning. Given that limbic abnormalities are often observed in mood, anxiety,

and other psychiatric disorders, irregularities in hedonic ratings may also be a marker for psychiatric disorders (Atanasova, 2008). Deficits in other areas of olfaction, such as odor identification and detection threshold, are thought to represent a neurodegenerative process, and as such are more commonly seen in diagnoses such as Alzheimer’s disease, dementia, and schizophrenia (Atanasova, 2008).

A meta-analysis by Atanasova (2008) found that deficits in odor identification, recognition, and discrimination have been consistently observed in people with schizophrenia. Most studies included in the meta-analysis also found that people with schizophrenia reported lower hedonic ratings of odors, although a few actually reported higher ratings. These inconsistent findings could be explained by variability in rates of anhedonia (an inability to experience pleasure) across the samples (Atanasova, 2008), as individuals with more anhedonia may be less able to experience pleasure in response to pleasant odor. In the same meta-analysis, people with depression were found to experience certain pleasant smells, particularly those deemed “relaxing,” to be more pleasant than those without depression (Atanasova, 2008). This may be explained by activation of the orbitofrontal cortex in response to olfactory stimuli, due to its association with the hedonic aspect of odor evaluation (Savic, 2001).

In another study, Croy et al. (2014) tested odor discrimination, identification, intensity, and hedonic response, and examined neural activation in response to olfactory stimuli during fMRI in females with depression before and after undergoing inpatient psychotherapy and compared them to a group of female healthy controls. Prior to initiating psychotherapy, the group with depression demonstrated reduced odor discrimination ability and odor pleasantness ratings and showed less activation of

olfactory brain areas (thalamus, insula, and left orbitofrontal cortex), while smelling the odors. Post-psychotherapy, no significant differences were observed between the groups.

Another study investigated associations between the T & T olfactometer detection and identification threshold test, and anxiety (state and trait) in a Japanese sample. The authors found a negative correlation between identification threshold for the rose odor and state anxiety in males and females, however only males exhibited a similar association for trait anxiety (Takahashi et al., 2015).

Taken together, these research findings suggest that impairment in the processing of olfactory stimuli could be a potential marker for psychiatric disorders in general, with unique patterns existing within different diagnostic classifications (Atanasova, 2008). As such, further research is needed to determine if such impairments are present in DDD, which has not been studied in relation to olfactory processing.

Limbic abnormalities are commonly reported in psychiatric disorders, and given the olfactory system’s close connections with the limbic system, associations between psychiatric symptoms and abnormal olfactory hedonic ratings, threshold detection, and identification make theoretical sense. According to Blanchard, Blanchard, and Rosen

(2008), animal models of defensive processing of aversive olfactory stimuli (generally those associated with predators) may potentially be extended to human olfactory systems as well. In animals, aversive olfactory stimuli can become an unconditioned fear stimulus which may lead to anxiety and posttraumatic stress behaviors. Blanchard et al. (2008) suggests there may be a similar system linking olfaction and defensive processes to human psychopathologies such as panic and other anxiety disorders.

The Current Study

The present study aimed to explore possible relations between olfactory functioning and depersonalization symptoms. In particular, this study examined associations between perception of odorants and emotional response. Given that olfaction has close connections to the limbic system, and that prior research has shown abnormalities in olfactory processing in several psychiatric disorders such as depression and anxiety, such abnormalities may also be present in DDD. The summarized evidence above suggests that limbic abnormalities are present in DDD. The disorder is also highly co-morbid with depression and anxiety disorders (APA, 2013), which are similarly associated with abnormal limbic functioning. Individuals with DDD tend to experience emotional numbing paired with heightened sensory awareness, which gives rise to a subjective feeling of unreality (Simeon, 2004). This is different from anhedonia typically reported in depression and schizophrenia in that it is not simply an inability to experience pleasure, but a flattening of all emotional experiences both positive and negative. Due to this emotional numbing and the evidence suggesting hedonic ratings of odor may be related to limbic functioning, abnormal ratings of both pleasantness and unpleasantness of odors may act as a marker for DDD and/or the presence of sub-clinical symptoms. As well, several sensory areas of the brain responsible for vision, audition, and somatosensory functioning have been implicated in DDD (Simeon et al., 2001).

Individuals with DDD frequently complain of feeling “numb,” and often describe unusual visual or auditory perception. Given that DDD is a diagnosis which affects both sensory and emotional processing, and olfaction has strong links to both, olfactory functioning may be a marker for DDD. Thus, the following hypotheses were tested:

Hypothesis 1: Odor identification ability will be negatively correlated with reported depersonalization/derealization symptoms.

Hypothesis 2: Odor detection threshold will be positively correlated with depersonalization/derealization symptoms.

Hypothesis 3: Hedonic ratings of both pleasantness and unpleasantness of odors will be negatively correlated with depersonalization/derealization symptoms.

CHAPTER 2

METHODS

Participants

The sample included 33 male and 59 female undergraduate students (N = 92) enrolled at a moderately sized private Midwestern university. Participants were enrolled in psychology courses and received research credit in exchange for their participation.

The age range of participants was 18 to 24 (M = 19.75, SD = 1.43). Race and ethnicity data were not collected to protect participant confidentiality as the majority of students at the university are Caucasian. Only one participant endorsed daily cigarette smoking and four participants endorsed occasional cigarette smoking. None had smoked on the day they participated.

Measures

Depersonalization/Derealization. The Cambridge Depersonalization Scale (CDS;

Sierra & Berrios, 2000; see Appendix A), is a 29 item self-report measure of both the frequency and duration of depersonalization and derealization symptoms. For each scale item presented, the measure asks participants to rate frequency of symptoms on a scale of zero (never) to four, (all the time); and duration of symptoms on a scale of one (a few seconds) to six (more than one week). Scores can range from 29 to 290, with a recommended cut-off point of 70 as an indicator of clinically significant depersonalization. The scale has good internal consistency (α = 0.89) and split-half 16

reliability (r = 0.92). Test-retest reliability (r = 0.39) is only available for a

Spanish language version of the scale (Molina et al., 2006). Convergent validity was established by comparing CDS scores with the Dissociative Experiences Scale (r = 0.49).

Discriminant validity was established by comparing CDS scores to the Beck Depression

Inventory (r = 0.15), and Zung Anxiety Scale (r = 0.03). These scores suggest good construct validity (Sierra & Berrios, 2000).

Anxiety. The Generalized Anxiety Disorder 7-Item Scale (GAD-7; Spitzer et al.,

2006; see Appendix B) is a self-report measure of anxiety symptoms. The measure contains seven items, each of which ask participants to rate anxiety symptoms within a two-week period on a scale from zero (not at all) to three (nearly every day). Scores can range from 0 to 21, with higher scores denoting more severe anxiety. The GAD-7 has shown good reliability. Internal consistency was demonstrated (α = 0.92), as was test- retest reliability (r = 0.83). Convergent validity was established by comparing GAD-7 scores to two related measures, the Beck Anxiety Inventory (r = 0.72), and anxiety subscales of the Symptom Checklist-90 (r = 0.74), suggesting good construct validity

(Spitzer et al., 2006).

Depression. The Center for Epidemiologic Studies Depression Scale-Revised

(CESD-R; Radloff, 1977; Eaton, Muntaner, Smith, Tien, & Ybarra, 2004; see Appendix

C) is a self-report measure of depression symptoms developed for the general population.

The scale consists of 20 items, each of which ask participants to rate depression symptoms within a two-week period on a scale from zero (not at all or less than one day) to four (nearly every day). Scores can range from 0 to 60, with higher scores denoting more severe depression. The CES-D-R has shown good reliability (Cronbach’s alpha

ranges from α = 0.87 to α = 0.98). Correlation coefficients with the original CES-D range from r = 0.88 to r = 0.93 (Eaton et al., 2004).

Olfaction. Sniffin’ Sticks (Hummel, Sekinger, Wolf, Pauli, & Kobal, 1997) is a test of olfactory functioning which utilizes pen-like odor dispensers to measure odor detection sensitivity and odor identification. Odor sensitivity is measured with dispensers containing gradated levels of n-butanol, presented alongside two decoy dispensers containing water. The participant is asked to identify which of the three contains the odor.

Pens are presented in ascending order until the participant is able to correctly identify the odorant twice. When the participant does so, pens are then presented in descending order until the participant makes an error, wherein the process is reversed. After seven repetitions, the last four reversal point scores are averaged to determine the odor detection sensitivity score. Higher numerical scores denote higher sensitivity to odor detection (Hummel et al., 1997).

Odor identification is measured with similar pen-like dispensers containing 16 different odorants. The participant is asked to identify each odor from four choices presented by the researcher. Examples of the sixteen assessed odors include banana, coffee, and fish (Hummel et al., 1997).

Test-retest reliability is acceptable for both the Identification (r’s range from 0.61 to 0.88) and Threshold (r’s range from 0.73 to 0.91) tests (Hummel et al., 1997; Haehner et al., 2009). Convergent validity was established with the University of Pennsylvania

Smell Identification Test (UPSIT) for both the Sniffin’ Sticks Identification (r = 0.85) and Threshold (r = 0.91) tests (Wolfensberger, Schnieper, & Welge-Lüssen, 2000).

Hedonic Odor Ratings. During the identification test, participants were asked how pleasant and how unpleasant they find each dispensed odor. The pleasantness and unpleasantness of each odor was assessed with two five-point Likert scales which ask the participant to rate the pleasantness and unpleasantness of each odor, where 1 = not pleasant and 5 = extremely pleasant for the pleasantness scale, and 1 = not unpleasant and

5 = extremely unpleasant for the unpleasantness scale (see Appendix D).

Design and Procedures

Participants were run individually, and first informed of the procedures and purpose of the experiment and asked to sign an informed consent. Participants were then asked to answer demographics questions which included age, sex, smoking status, length of time since the last cigarette, and date of most recent menstrual cycle if the participant was female. Participants then underwent testing of odor detection threshold, followed by odor identification ability and olfactory hedonics. When the odor identification task was completed, participants were asked to complete the GAD-7, CES-D-R, and CDS by hand.

Participants were then debriefed, and research credit granted.

CHAPTER 3

RESULTS

Preliminary Analyses

All analyses were conducted using SPSS statistical software version 23. Mean scores, standard deviations, and range of scores for all continuous measures are presented in Table 1. The majority of participants experienced relatively low levels of depression

(CESD-R < 16), depersonalization (CDS < 70), and anxiety (GAD-7 < 5). Internal consistency for the questionnaires were as follows: CESD-R α = .88, GAD-7 α = .86,

CDS α = .93. Skewness and kurtosis (presented in Table 2) of all primary variables were analyzed. Correlations between primary variables (presented in Table 3) were found to be nonsignificant, with the exception of the psychological measures, which all correlated with one another. Odor pleasantness ratings were also found to significantly correlate with odor identification

Table 1

Means and Standard Deviations for All Measures

n M(SD) CDS 92 53.2(19.2) GAD-7 92 6.5(4.5) CESD-R 92 13.9(8.9) Identification 92 11.3(1.8) Threshold 92 7.8(2.1) Unpleasantness 92 24.0(7.4) Pleasantness 92 19.0(7.6) 20

Table 2

Tests of Normality (N=92)

Skewness(SE) Kurtosis(SE) CDS 1.28(.251) 1.83(.498) CESD-R 1.06(.253) 1.03(.500) GAD-7 1.10(.251) .975(.498) Identification -.277(.251) -.087(.498) Threshold .309(.251) .733(.498) Unpleasantness .354(.251) .092(.498) Pleasantness .017(.251) .658(.498)

Table 3

Correlation Table (N=92)

1 2 3 4 5 6 7 8

1.CDS - .615** .438** -.164 .037 .024 .010 .173

2. CESD-R - - .728** -.117 .043 .078 -.012 -.006

3. GAD-7 - - - -.133 .072 .190 -.003 -.128

4. Identification - - - - -.017 -.145 .242* .127

5. Threshold - - - - - .019 .072 .124

6.Unpleasantness ------.087 .020

7. Pleasantness ------.083

8. Age ------

Primary Analyses

Results are presented by hypothesis. Exploratory analyses are presented in a subsequent section, also separated by the three hypotheses tested.

Hypothesis 1. Linear multiple regression was used to test whether depersonalization symptoms predict odor identification ability, when controlling for anxiety and depression. The results (presented in Table 4) indicated that CDS scores did not significantly predict odor identification scores (β = -.164, t = -1.22, p = .224.)

Table 4 Results of Multiple Regression Analyses- Odor Identification (N=92) Model Predictor b SE β t p R² F(p) Variables 1(Identification) (constant) 12.14 .551 - 22.04 .000 - - CDS -.015 .012 -.164 -1.22 .224 - - GAD-7 -.041 .061 -.105 -.680 .498 - - CESD-R .012 .035 .062 .365 .723 - - .035 1.04(.380)

Hypothesis 2. A linear multiple regression analysis was used to test whether depersonalization symptoms predicted odor threshold detection, when controlling for anxiety and depression. The results (presented in Table 5) indicated that CDS scores did not significantly predict odor detection threshold when (β = .001, t = .009, p = .992.).

Table 5 Results of Multiple Regression Analyses- Threshold Detection (N=92) Model Predictor b SE β t p R² F(p) Variables 2(Threshold) (constant) 7.57 .663 - 11.42 .000 - - CDS .000 .015 .001 .009 .992 - - GAD-7 -.010 .073 -.021 -.135 .893 - - CESD-R .014 .042 .058 .324 .747 - - .042 .060(.980)

Hypothesis 3. Linear multiple regression was used to test whether depersonalization symptoms predicted odor unpleasantness and pleasantness ratings, with anxiety and depression included as covariates. The results (presented in Table 6) indicated that CDS scores did not significantly predict unpleasantness (β = -.044, t = -

.326, p = .745.) or pleasantness ratings (β = .028, t = .206 p = .837.)

Table 6

Results of Multiple Regression Analyses- Unpleasantness and Pleasantness Ratings (N=92) Model Predictor b SE β t p R² F(p) Variables 3(Unpleasantness) (constant) 17.97 2.38 - 7.56 .000 - - CDS -.017 .053 -.044 -.326 .745 - - GAD-7 .403 .263 .236 1.53 .129 - - CESD-R -.057 .150 -.067 -.381 .704 - - .034 1.01(.394) 4(Pleasantness) (constant) 23.72 2.35 - 10.01 .000 - - CDS .011 .052 .028 .206 .837 - - GAD-7 .020 .260 .012 .077 .939 - - CESD-R -.031 .148 -.038 -.211 .833 - - .001 .020(.996)

Exploratory Analyses

Sex Differences. Due to the sexually dimorphic nature of the olfactory system

(Stockhorst & Pietrowsky, 2004), sex differences were also analyzed by hypothesis.

Means, standard deviations, and range of scores are presented separately by sex in Table

7. Independent samples t-tests for all measures (presented in Table 8) revealed no significant mean differences. For hypothesis 1, significant sex differences were observed.

The results (presented in Tables 9 and 10) showed that when controlling for anxiety and depression, CDS scores significantly predicted odor identification scores in females (β = -

.339, t = -2.06, p = .044) but not in males (β = .266, t = 1.20, p = .240). The overall model was not significant at the p = .05 level.

Table 7

Means and Standard Deviations for all Measures, by Sex

Males Females n M(SD) n M(SD) CDS 33 39.7(7.1) 59 39.1(12.0) GAD-7 33 5.4(3.6) 59 7.2(4.9) CESD-R 33 13.8(8.0) 59 13.9(1.8) Identification 33 10.9(1.7) 59 11.5(1.8) Threshold 33 8.0(2.2) 59 7.7(2.1) Unpleasantness 33 18.2(7.5) 59 19.4(7.8) Pleasantness 33 22.5(7.5) 59 24.8(7.2)

Table 8

Independent Samples T-Tests for all Measures, by Sex

n t(df) p CDS 92 .659(90) .513 GAD-7 92 -1.86(90) .066 CESD-R 92 -038(89) .970 Identification 92 -1.49(90) .141

Threshold 92 .524(90) .602 Unpleasantness 92 -.746(90) .458 Pleasantness 92 -1.45(90) .151

Table 9 Results of Multiple Regression Analyses in Males- Odor Identification (N=33) Model Predictor b SE β t p R² F(p) Variables 1(Identification) (constant) 9.93 1.11 - 9.00 .000 - - CDS .027 .023 .266 1.20 .240 - - GAD-7 -.021 .137 -.037 -.150 .882 - - CESD-R -.035 .058 -.165 -.595 .557 - - .052 .510(.678)

Table 10 Results of Multiple Regression Analyses- Females (N=59) Model Predictor b SE β t p R² F(p) Variables 1(Identification) (constant) 12.95 .615 - 21.05 .000 - - CDS -.029 .014 -.339 -2.06 .044* - - GAD-7 -.095 .073 -.263 -1.30 .200 - - CESD-R .051 .043 .272 1.19 .238 - - .119 2.47(.072)

For hypothesis 2, results (presented in tables 11 and 12) did not change significantly when analyzed separately by sex. CDS scores did not significantly predict odor threshold detection in either males (β = -.048, t = -.210, p = .835) or females (β =

.023, t = .129, p = .898).

Table 11 Results of Multiple Regression Analyses in Males- Threshold Detection (N=33) Model Predictor b SE β t p R² F(p) Variables 2(Threshold) (constant) 7.80 1.35 - 5.76 .000 - - CDS -.006 .028 -.048 -.210 .835 - - GAD-7 .036 .167 .054 .214 .832 - - CESD-R .007 .071 .030 .104 .918 - - .005 .045(.987)

Table 12 Results of Multiple Regression Analyses in Females- Threshold Detection (N=59) Model Predictor b SE β t p R² F(p) Variables 2(Threshold) (constant) 7.47 .789 - 9.47 .000 - - CDS .002 .018 .023 .129 .898 - - GAD-7 -.019 .094 -.043 -.199 .843 - - CESD-R .015 .055 .065 .266 .791 - - .003 .056(.982)

For hypothesis 3, results (presented in Tables 13 and 14) did not significantly change for either unpleasantness or pleasantness ratings. CDS scores did not predict unpleasantness ratings in males or females (male: β = .103, t = .486, p = .631; female: β =

-.078, t = -.462, p = .646) or pleasantness (male: β = .169, t = .761, p = .453; female: β = -

.008, t = -.045, p = .964).

Table 13 Results of Multiple Regression Analyses in Males- Unpleasantness and Pleasantness Ratings (N=33) Model Predictor b SE β t p R² F(p) Variables 3(Unpleasantness) (constant) 11.52 4.44 - 2.60 .015 - - CDS .044 .091 .103 .486 .631 - - GAD-7 .131 .547 .056 .240 .812 - - CESD-R .235 .234 .265 1.00 .324 - - .138 1.50(.237) 4(Pleasantness) (constant) 17.85 4.97 - 3.60 .001 - - CDS .077 .102 .169 .761 .453 - - GAD-7 .556 .612 .223 .908 .371 - - CESD-R -.175 .262 -.186 -.669 .509 - - .049 .480(.699)

Table 14 Results of Multiple Regression Analyses in Females- Unpleasantness and Pleasantness (N=59) Model Predictor b SE β t p R² F(p) Variables 3(Unpleasantness) (constant) 19.99 2.82 - 7.07 .000 - - CDS -.030 .064 -.078 -.462 .646 - - GAD-7 .612 .334 .384 1.83 .072 - - CESD-R -.242 .196 -.290 -1.23 .222 - - .062 1.22(.313) 4(Pleasantness) (constant) 25.81 2.65 - 9.75 .000 - - CDS -.003 .060 -.008 -.045 .964 - - GAD-7 -.284 .314 -.194 -.905 .369 - - CESD-R .085 .184 .111 .462 .646 - - .017 .313(.816)

Further exploratory analyses were conducted to analyze simple and interaction effects of sex and depersonalization on odor identification, odor detection threshold, and odor pleasantness and unpleasantness ratings. Participants were grouped into high depersonalization (CDS ≥ 50) and low depersonalization (CDS ≤ 49), so that means could be compared. These cutoffs were chosen based on the sample median CDS score.

Each outcome variable was entered into a 2 (depersonalization group: high versus low) by 2 (sex: male vs female) ANOVA. Anxiety and depression were controlled for.

For hypothesis 1, main effects for sex (F(1, 85) = 3.46, p = .066) and depersonalization group (F(1, 85) = .530, p = .185) were not significant. However, a significant sex by depersonalization group interaction was found, (F(1, 85) = 5.50, p =

.021), indicating that females in the high depersonalization group had significantly lower odor identification scores. These findings are consistent with the regression analyses.

Mean differences of the sex by depersonalization group interaction are displayed in Table

15.

Table 15 Mean Differences for Sex x Depersonalization Group Interaction

Low Depersonalization High Depersonalization n M(SE) n M(SE) Male 16 10.50 (1.97) 16 11.19 (1.38) Female 30 12.07 (1.41) 29 10.86 (1.90)

For hypothesis 2, main effects for sex (F(1, 85) = .056, p = .813) and depersonalization group (F(1, 85) = .005-, p = .946), on odor detection threshold were not significant. The sex by depersonalization group interaction was not significant (F(1, 85) =

.610, p = .437).

For hypothesis 3, main effects for sex (F(1, 85) = .150, p = .700) and depersonalization group (F(1, 85) = .011-, p = .917), on odor unpleasantness ratings were not significant and there was no sex by depersonalization group interaction (F(1, 85) = .318, p = .574).

Similarly, main effects for sex (F(1, 85) = 2.02, p = .159) and depersonalization group

(F(1, 85) = .584, p = .447), on odor pleasantness ratings were not significant., with no sex by depersonalization group interaction (F(1, 85) = 1.57, p = .214).

CHAPTER 4

DISCUSSION

The goal of the present study was to examine possible links between depersonalization symptoms and olfactory functioning. It was hypothesized that higher levels of reported depersonalization would be negatively correlated with odor identification ability, positively correlated with odor threshold detection, and negatively correlated with odor hedonic ratings. None of the primary hypotheses were supported.

However, due to the unexpectedly healthy nature of the sample, no definitive conclusions may be drawn.

Depersonalization was not associated with odor identification ability. Odor identification is concerned primarily with the perception and recognition of the odorants presented, which we expected to be lower in those with higher levels of depersonalization. People with DDD have been shown to experience abnormalities in brain areas related to the perception of sensory information (Simeon et al., 2001). As well, defining markers of DDD include abnormal perceptions of sensory input. In particular, the symptom of derealization is defined by perceiving external sensations as unreal (Baker et al., 2003). As such, we expected olfactory functioning to also be affected. However, our data did not provide support for a relationship between smell identification and the perceptual abnormalities related to depersonalization. It is possible

that depersonalization has a greater impact on the visual, auditory, and tactile systems, and that the perception of chemical senses is not affected. It is also possible that our undergraduate sample, which had lower than expected DDD symptom levels, did not have enough variability to detect a real relationship between odor identification and depersonalization.

Depersonalization was also not associated with odor detection threshold. The odor detection threshold test measured actual sensory ability of participants, which we expected to be lower in those with higher levels of depersonalization. In those with DDD, the exact nature of abnormal sensations is unclear. Subjective complaints can range from seeming to sense too much, to not sensing enough at all (Baker et al., 2003). However, whether these complaints result from abnormalities in sensation or in the perception of normal sensory input is not well understood. A significant finding for this hypothesis might have clarified the relationship. Given our data, which showed correlations close to zero, it appears likely that sensory processing remains normal in those with higher levels of DDD. This would suggest that observed symptoms are more likely the result of abnormal perception, rather than sensation. Replication in clinical samples would better determine if the relationship genuinely does not exist.

Depersonalization was not related to either odor unpleasantness or pleasantness ratings. We expected to find that the emotional ratings of odorants would be less intense in those with higher levels of depersonalization, as depersonalization is characterized by a state of emotional numbing (Simeon, 2004). Olfaction is generally observed as being highly related to emotional processing (Stockhorst & Pietrowsky, 2004), in large part due to its close association with the amygdala (Ledoux, 1997), so the lack of any observable

relationship was surprising. However, the onset of depersonalization symptoms often occurs midway through adolescence, at which point hedonic values of common odorants may have already been encoded in the brain. Memories associated with smell have been shown to be longer lasting, and smell may trigger older memories (Willander & Larsson,

2007). It may be the case that depersonalization does not affect the hedonic valences of odorants, because participants had preconceived ideas of how pleasant or unpleasant they felt odorants were prior to the onset of symptoms. As with all our hypotheses, however, it is also possible that our findings are limited by the sample, and effects might be observed with a clinical sample. Adequate conclusions may not be drawn due to these limitations.

Despite the non-significance of our primary hypotheses, sex stratified exploratory analyses provided a more nuanced understanding of these results. Consistent with the first hypothesis, depersonalization was negatively correlated with odor identification ability in females; however, depersonalization and odor identification were not correlated in males. This suggests females with higher levels of depersonalization may be impaired in their ability to identify odor. As well, when we split groups into low and high depersonalization scores, a significant sex by depersonalization group interaction was observed, which showed females were scoring significantly lower on odor identification than males when they were experiencing higher levels of depersonalization.

It also appeared that anxiety symptoms may be related to odor unpleasantness ratings in females, although the finding was only significant at the trend level of p < .10.

The trend was positive, however, suggesting that higher anxiety might be related to higher unpleasantness ratings. These results suggest that anxiety may more strongly

predict odor hedonic valence than depersonalization, but additional research is needed to confirm this finding

No relationship was found for odor pleasantness ratings or odor threshold detection in either sex, suggesting that both threshold detection and pleasantness ratings are not associated with depersonalization. In regards to threshold detection, while depersonalization has shown over and under-activation in major sensory and perceptual areas of the brain (Simeon et al., 2001), olfaction was not studied directly. It is largely possible that the sensory ability to detect odorants is not impaired in DDD.

With regard to pleasantness ratings, it may be the case that, despite emotional impairments being common to depersonalization symptoms, the ability to identify odorants as pleasant remains intact. This might be a result of strong odor memory, which likely preceded onset of symptoms, creating a pleasant association that is not affected by

DDD. As olfactory memories tend to have unusually strong emotional components and create more potent memories than other sensory stimuli (Willander & Larsson, 2007), it may be the case that these pre-existing memories and associations simply override the effect of depersonalization symptoms. It may also be the case that differences in neural processing of pleasant versus unpleasant stimuli may mean that the processing of pleasant odors is not affected by DDD. While unpleasant affect is largely processed via the amygdala, pleasant affect is projected upwards to the ventral striatum and nucleus accumbens (Cardinal, Parker, Hall, & Everitt, 2002), which may not be affected by DDD.

Given that the neural mechanisms of DDD are not well understood, further research would need to clarify whether or not the ventral striatum is at all impacted by DDD.

A major limitation of this study was the use of an undergraduate student sample at a private university. Based on a previous study (Aderibigbe et al., 2003) and DSM-5 prevalence rates (APA, 2013) it was expected that approximately 20-25 percent of the university student sample would endorse clinically significant symptoms. However, in the present study only 18 percent of the participants scored in the clinical range (> 70) on the CDS. This may have affected results due to an overabundance of participants with a normal range of depersonalization symptoms. Of note, scores on the CESD-R and GAD-

7 were also generally lower than what might have been expected, even in a sample of undergraduate students. It is possible that undergraduate students in this sample report less psychological impairment than would be expected for college students.

Future studies examining the relation between olfaction and depersonalization would benefit from the use of a clinical sample. Comparison between those diagnosed with DDD and other psychiatric diagnoses, as well as a sample of healthy participants, would be largely beneficial in exploring the effects of depersonalization on olfactory processing.

Potential reasons for these findings are variable. However, it is worth noting that while none of the analyses were significant, some were trending in a direction that could show promise in future research. However, the possibility that depersonalization symptoms are not related to olfactory processing must also be considered. While it does appear that odor identification ability is associated with depersonalization symptoms in females, further study would help clarify these sex differences. Possible reasons for such differences may include the sexually dimorphic nature of the vomeronasal system, or possible sex differences in the way odor memory is processed in males versus females. It

may also be the case that depersonalization affects the female brain in slightly different ways than the male brain, with odor identification being only one of a myriad number of observable differences.

As this research is largely correlational in nature, causal factors cannot be determined. Hypotheses could neither be confirmed nor disconfirmed due to the limitations of the sample used. A replication of this study using a clinical sample would be more likely to clarify our understanding of the observed association. Further research is also needed to determine whether or not any relationship between depersonalization symptoms and olfactory processing would exist in a clinical sample, where the findings could be most relevantly applied. As well, clinical samples might show significant findings that were not observed in this study.

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APPENDIX A

Cambridge Depersonalization Scale (CDS)

Please read these instructions carefully: this questionnaire describes strange and ‘funny’ experiences that normal people may have in their daily life. We are interested in the experiences’ frequency – how often you have had these experiences over the last six months, and their approximate duration. To the right of each question please fill in a number that estimates how frequently (use 0–4 scale given below) you estimate you have had this symptom over the last six months, and how long (use 0–6 scale below) on average the symptom has tended to last for. If not sure, give your best guess. Please use the following scales: frequency: 0 = never; 1 = rarely; 2 = often; 3 = very often; 4 = all the time duration: (on average it lasts): 1 = few seconds; 2 = few minutes; 3 = few hours; 4 = about a day; 5 = more than a day; 6 = more than a week

Questions Frequency Duration

Out of the blue I feel strange, as if I were not real or as if I were cut off from the world. What I see looks flat or lifeless, as if I were looking at a picture.

Parts of my body as if they didn’t belong to me.

I have found myself not being frightened at all in situations which normally I would find frightening or distressing. My favorite activities are no longer enjoyable.

While doing something, I have the feeling of being a “detached observer” of myself. The flavor of meals no longer gives me a feeling of pleasure or distaste. My body feels very light, as if I were floating on air.

I have the feeling of not having any thoughts at all, so that when I speak it feels as if my words were being uttered by an “automaton.” 42

Familiar voices (including my own) sound remote and unreal.

I have the feeling that my hands or my feet have become larger or smaller. My surroundings feel detached or unreal, as if there were a veil between me and the outside world. It seems as if things that I have recently done had taken place a long time ago. For example, anything which I have done this morning feels as if it were done weeks ago. While fully awake, I have “visions” in which I can see myself outside, as if I were looking at my image in a mirror. When in a new situation, it feels as if I have been through it before.

Objects around me seem to look smaller or further away.

I cannot feel properly the objects that I touch with my hands, for it feels as it were not me who were touching it. I do not seem able to picture things in my mind, for example, the face of a close friend or a familiar place. When a part of my body hurts, I feel so detached form that pain that it feels as if it were somebody else’s pain. I have the feeling of being outside my body.

When I move it doesn’t feel as if I were in charge of the movements, so that I feel “automatic” and “mechanical,” as if I were a robot. The smell of things no longer gives me a feeling of pleasure or dislike. I feel so detached from my thoughts that they seem to have a life of their own. I have to touch myself to make sure that I have a body or a real existence. I seem to have lost some bodily sensations (e.g., of hunger and thirst) so that when I eat or drink, it feels like an automatic routine. Previously familiar places look unfamiliar, as if I had never seen them before.

APPENDIX B

Generalized Anxiety Disorder 7-Item Scale (GAD-7)

Over the last 2 weeks, how often have Not at Several Over half Nearly you been bothered by the following all sure days the days every day problems?

Feeling nervous, anxious, or on edge. 0 1 2 3

Not being able to stop or control 0 1 2 3 worrying.

Worrying too much about different 0 1 2 3 things.

Trouble relaxing. 0 1 2 3

Being so restless that it’s hard to sit 0 1 2 3 still.

Becoming easily annoyed or irritable. 0 1 2 3

Feeling afraid if something awful 0 1 2 3 might happen.

If you checked off any problems, how difficult have these made it for you to do your work, take care of things at home, or get along with other people?

Not difficult at all Somewhat difficult Very difficult Extremely difficult

APPENDIX C

Center for Epidemiologic Scale for Depression, Revised

Below is a list of the ways you might have felt or behaved. Please indicate how often you have felt this way in the past week or so.

Not at all Nearly or less 1-2 days 3-4 days 5-7 days every day than 1 day for 2 weeks

My appetite was poor. 0 1 2 3 4

I could not shake off the 0 1 2 3 4 blues.

I had trouble keeping my 0 1 2 3 4 mind on what I was doing.

I felt depressed. 0 1 2 3 4

My sleep was restless. 0 1 2 3 4

I felt sad. 0 1 2 3 4

I could not get going. 0 1 2 3 4

Nothing made me happy. 0 1 2 3 4

I felt like a bad person. 0 1 2 3 4

I lost interest in my usual 0 1 2 3 4 activities.

I slept much more than 0 1 2 3 4 usual.

I felt like I was moving too 0 1 2 3 4 slowly.

I felt fidgety. 0 1 2 3 4

I wished I were dead. 0 1 2 3 4

I wanted to hurt myself. 0 1 2 3 4

I was tired all the time. 0 1 2 3 4

I did not like myself. 0 1 2 3 4

I lost a lot of weight 0 1 2 3 4 without trying to.

I had a lot of trouble 0 1 2 3 4 getting to sleep.

I could not focus on the 0 1 2 3 4 important things.

APPENDIX D

Odor Hedonic Rating Scales

How Pleasant is this Odor? Not Pleasant A Little Pleasant Very Pleasant Extremely Pleasant Pleasant 1 2 3 4 5

How Unpleasant is this Odor? Not Unpleasant A Little Unpleasant Very Extremely Unpleasant Unpleasant Unpleasant 1 2 3 4 5