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Sleep Predicts Task Negative Brain Activity in Fibromyalgia Participants with Chronic Insomnia

Permanent Link: http://ufdc.ufl.edu/UFE0045460/00001

Material Information

Title: Sleep Predicts Task Negative Brain Activity in Fibromyalgia Participants with Chronic Insomnia
Physical Description: 1 online resource (48 p.)
Language: english
Creator: Vatthauer, Karlyn E
Publisher: University of Florida
Place of Publication: Gainesville, Fla.
Publication Date: 2013

Subjects

Subjects / Keywords: comorbid -- fibromyalgia -- functional -- insomnia -- neuroimaging
Clinical and Health Psychology -- Dissertations, Academic -- UF
Genre: Psychology thesis, M.S.
bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract: Approximately 75% of fibromyalgia patients also have chronic insomnia. The Cognitive Activation Theory of Stress (CATS) provides a possible explanation for this high comorbidity rate. Specifically,CATS posits subjective health complaints (fibromyalgia, insomnia) are caused by sustained psychophysiological response to a previously normal physiological process (pain, poor sleep). Continued increased arousal causes the central nervous system (CNS) to become sensitized to the stimuli, and ultimately dysregulated following persistent sensitization. The present study investigated whether sleep disturbance indicators total sleep time-TST, total wake time-TWT predict increased basal brain activation (indicator of dysregulation) in individuals with fibromyalgia and insomnia (FMI) compared to those with fibromyalgia only (FM). We hypothesized decreased TST and increased TWT would be accompanied by increased basal brain activation of primarily emotional response,somatosensory, conscious evaluation, and pain processing areas in FMI compared to FM. Thirty-three adults completed 14 days of sleep diaries prior to an fMRI protocol. A whole-brain GLM analysis examined brain areas associated with greater basal brain activity predicted by TST and TWT during task negative periods in both groups. TST was associated with increased basal brain activation in pain processing, emotion, and somatosensory-related areas, while TWT was associated with increased basal brain activation in language, pain processing, sleep regulation, planning, and consciousness areas in FMI compared to FM. Future work will investigate the potentially additive effects of brain activation in the regions identified in this study and will investigate whether increased basal brain activity can be ‘corrected’ by cognitive-behavioral therapies for insomnia and pain.
General Note: In the series University of Florida Digital Collections.
General Note: Includes vita.
Bibliography: Includes bibliographical references.
Source of Description: Description based on online resource; title from PDF title page.
Source of Description: This bibliographic record is available under the Creative Commons CC0 public domain dedication. The University of Florida Libraries, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.
Statement of Responsibility: by Karlyn E Vatthauer.
Thesis: Thesis (M.S.)--University of Florida, 2013.
Local: Adviser: Mccrae, Christina Smith.
Electronic Access: RESTRICTED TO UF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE UNTIL 2015-05-31

Record Information

Source Institution: UFRGP
Rights Management: Applicable rights reserved.
Classification: lcc - LD1780 2013
System ID: UFE0045460:00001

Permanent Link: http://ufdc.ufl.edu/UFE0045460/00001

Material Information

Title: Sleep Predicts Task Negative Brain Activity in Fibromyalgia Participants with Chronic Insomnia
Physical Description: 1 online resource (48 p.)
Language: english
Creator: Vatthauer, Karlyn E
Publisher: University of Florida
Place of Publication: Gainesville, Fla.
Publication Date: 2013

Subjects

Subjects / Keywords: comorbid -- fibromyalgia -- functional -- insomnia -- neuroimaging
Clinical and Health Psychology -- Dissertations, Academic -- UF
Genre: Psychology thesis, M.S.
bibliography   ( marcgt )
theses   ( marcgt )
government publication (state, provincial, terriorial, dependent)   ( marcgt )
born-digital   ( sobekcm )
Electronic Thesis or Dissertation

Notes

Abstract: Approximately 75% of fibromyalgia patients also have chronic insomnia. The Cognitive Activation Theory of Stress (CATS) provides a possible explanation for this high comorbidity rate. Specifically,CATS posits subjective health complaints (fibromyalgia, insomnia) are caused by sustained psychophysiological response to a previously normal physiological process (pain, poor sleep). Continued increased arousal causes the central nervous system (CNS) to become sensitized to the stimuli, and ultimately dysregulated following persistent sensitization. The present study investigated whether sleep disturbance indicators total sleep time-TST, total wake time-TWT predict increased basal brain activation (indicator of dysregulation) in individuals with fibromyalgia and insomnia (FMI) compared to those with fibromyalgia only (FM). We hypothesized decreased TST and increased TWT would be accompanied by increased basal brain activation of primarily emotional response,somatosensory, conscious evaluation, and pain processing areas in FMI compared to FM. Thirty-three adults completed 14 days of sleep diaries prior to an fMRI protocol. A whole-brain GLM analysis examined brain areas associated with greater basal brain activity predicted by TST and TWT during task negative periods in both groups. TST was associated with increased basal brain activation in pain processing, emotion, and somatosensory-related areas, while TWT was associated with increased basal brain activation in language, pain processing, sleep regulation, planning, and consciousness areas in FMI compared to FM. Future work will investigate the potentially additive effects of brain activation in the regions identified in this study and will investigate whether increased basal brain activity can be ‘corrected’ by cognitive-behavioral therapies for insomnia and pain.
General Note: In the series University of Florida Digital Collections.
General Note: Includes vita.
Bibliography: Includes bibliographical references.
Source of Description: Description based on online resource; title from PDF title page.
Source of Description: This bibliographic record is available under the Creative Commons CC0 public domain dedication. The University of Florida Libraries, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.
Statement of Responsibility: by Karlyn E Vatthauer.
Thesis: Thesis (M.S.)--University of Florida, 2013.
Local: Adviser: Mccrae, Christina Smith.
Electronic Access: RESTRICTED TO UF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE UNTIL 2015-05-31

Record Information

Source Institution: UFRGP
Rights Management: Applicable rights reserved.
Classification: lcc - LD1780 2013
System ID: UFE0045460:00001


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1 SLEEP PREDICTS TASK NEGATIVE BRAIN ACTIVITY IN FIBROMYALGIA PARTICIPANTS WITH CHRONIC INSOMNIA By KARLYN ELIZABETH VATTHAUER A THESIS PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE UNIVERSITY OF FLORIDA 2013

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2 2013 Karlyn Elizabeth Vatthauer

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3 To my family for all their enco uragement, support, and prayers

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4 ACKNOWLEDGMENTS I would l ike to thank my mentor, Dr. Christina McCrae, for her support and guidance on this project. In addition, I want to thank Dr. Jason Craggs for his guidance in the neuroimaging portion of this project. Further, I want to recognize the members of my superviso ry committee: Dr. Michael Marsiske, Dr. David Janicke, and Dr. Deidre Pereira. I also want to thank Christine Towler (Lab Coordinator) ; Brittany Telford and Zac Zedar (Polysomnography Assistant s ) ; Susan Purdy (Polysomnography Technologist) ; Jacob Williams M.S., Daniela Roditi, M.S., and Ryan Anderson, M.S. (Graduate Assistant Study Therapists) ; and Janelle Letzen, B. S. (Neuroimaging Support) for their contribution s to this research project. Finally, I thank God for His guidance and blessings while pursui ng this degree. Study support was provided by Award Number R01AR055160 and R01AR055160 S1 ARRA Supplement from the National Institute of Arthritis And Musculoskeletal And Skin Diseases (Christina S. McCrae, PhD., PI; Michael E. Robinson, Ph.D., co PI).

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5 TABLE OF CONTENTS page ACKNOWLEDGMENTS ................................ ................................ ................................ .. 4 LIST OF TABLES ................................ ................................ ................................ ............ 7 LIST OF FIGURES ................................ ................................ ................................ .......... 8 LIST OF ABBREVIATIONS ................................ ................................ ............................. 9 ABSTRACT ................................ ................................ ................................ ................... 10 CHAPTER 1 INTRODUCTION ................................ ................................ ................................ .... 12 Fibromyalgia ................................ ................................ ................................ ........... 12 Chronic Insomnia ................................ ................................ ................................ .... 13 Sleep Disturbances, Changes in Sleep, and Pain ................................ .................. 14 Cognitive Activat ion Theory of Stress ................................ ................................ ..... 15 Previous Neuroimaging Research ................................ ................................ .......... 16 Present Study ................................ ................................ ................................ ......... 17 2 METHODS ................................ ................................ ................................ .............. 18 Recruitment ................................ ................................ ................................ ............ 18 Sample ................................ ................................ ................................ .................... 20 Experimental Ma terials ................................ ................................ ........................... 20 Measures ................................ ................................ ................................ ................ 21 Sleep Diaries ................................ ................................ ................................ .... 21 Clinical Pain ................................ ................................ ................................ ...... 21 Experimental Paradigm ................................ ................................ ........................... 22 f MRI Acquisition and Analysis ................................ ................................ ................. 22 Functional Da ta Reduction ................................ ................................ ...................... 23 3 RESULTS ................................ ................................ ................................ ............... 26 Independence of Sleep Disturbance Indicators ................................ ...................... 26 Between Group Heterogeneity ................................ ................................ ................ 26 Between Group Homogeneity ................................ ................................ ................. 26 Task Negative Brain Activity Group Differences ................................ ..................... 27 4 DISCUSSION ................................ ................................ ................................ ......... 34 APPENDIX : SLEEP DIARY ................................ ................................ .......................... 40

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6 LIST OF REFERENCES ................................ ................................ ............................... 42 BIOGRAPHICAL SKETCH ................................ ................................ ............................ 48

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7 LIST OF TABLES Table page 3 1 Coordinates for total sleep time regions with increased activation in the comorbid fibromyalgia and chronic insomnia (FMI) group compared to fibromyalgia only (FM) group ................................ ................................ .............. 29 3 2 Coordinates for total wake time regions with increased activation in the FMI group compared to FM only group ................................ ................................ ...... 30

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8 LIST OF FIGURES Figure page 2 1 Design of the functional runs, the total duration of which lasted 310 seconds. ... 25 3 1 Increased right inferior temporal gyrus activation in the FMI group compared to the FM group associated with TST. ................................ ................................ 31 3 2 Increased right medial temporal gyrus and bilateral precuneus activation in the FMI group compared to the FM group associated with TST. ....................... 31 3 3 Increased left and right superior frontal gyri activation in the FMI group compared to the FM group associated with TST. ................................ .............. 32 3 4 Increased right infer ior frontal gyrus activation in the FMI group compared to the FM group associated with TWT. ................................ ................................ ... 32 3 5 Increased right superio r and medial temporal gyri activation in the FMI group compared to the FM group associated with TWT. ................................ ............. 33 3 6 Increased right medial frontal gyrus activation in the FMI group compared to the FM group associated with TWT. ................................ ................................ ... 33

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9 LIST OF ABBREVIATIONS CATS Cognitive Activation Theory of Stress CNS Central Nervous System FM Fibromyalgia Only FMI Comorbid Fibromyalgia and Chronic Insomnia TST Total Sleep Time TWT Total Wake Time

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10 Abstract of Thesis Presented to the Graduate School of the University of Florida in Partial Fulfillment of the Requirements for the Degree of Master of Science SLEEP PREDICTS TASK NEGATIVE BRAIN ACTIVITY IN FIBROMYALGIA PARTICIPANTS WITH CHRONIC INSOMNIA By Karlyn Vatthauer May 2013 Chair: Christina Smith McCrae Major: Psychology Approximately 75% of fibromyalgia patients also have chronic insomnia. The Cognitive Activation Theory of Stress (CATS) provides a possible explanation for this high comorbidity rate. Specifical ly, CATS posits subjective health complaints (fibromyalgia, insomnia) are caused by sustained psychophysiological response to a previously normal physiological process (pain, poor sleep). Continued increased arousal causes the central nervous system (CNS) to become sensitized to the stimuli, and ultimately dysregulated following persistent sensitiz ation. The present study investigated whether sleep disturbance indicators [total sleep time TST, total wake time TWT] predict increased basal brain activation (i ndicat or of dysregulation) in individuals with fibromyalgia and insomnia (FMI) compared to those with fibromyalgia only (FM). We hypothesized decreased TST and increased TWT would be accompanied by increased basal brain activation of primarily emotional re sponse, somatosensory, conscious evaluation, and pain processing areas in FMI compared to FM. Thirty three adults completed 14 days of sleep diaries prior to an f MRI protocol. A whole brain GLM analysis examined brain areas associated with greater basal br ain activity predicted by

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11 TST and TWT during task negative periods in both groups. TST was associated with increased basal brain activation in pain processing, emotion, and somatosensory related areas, while TWT was associated with increased basal brain ac tivation in language, pain processing, sleep regulation, planning, and consciousness areas in FMI compared to FM. Future work will investigate the potentially additive effects of brain activation in the regions identified in this study and will investigate whether increased behavioral therapies for insomnia and pain.

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12 CHAPTER 1 INTRODUCTION Fibromyalgia Fibromyalgia, a highly prevalent and costly chronic pain syndrome, is associated with numerous general physical symptoms and increased rates of comorbidity with many other chronic conditions, including insomnia. Characterized by subjectively reported continuous, widespread pain for at least three months, fibromyalgia affects approximately 2% of American ad ults, with estimated annual direct and indirect costs of $29.7 billion ( Lawrence et al., 2008 ; Wolfe et al., 1997 ; Wolfe et al., 1990 ) T hese expenditures may also incorporate indirect costs of associated comorbidities as medical/psychiatric comorbidity is the strongest predictor of increased healthca re utilization in fibromyalgia ( Bernatsy, Dobkin, DeCivita, & Penrod, 2005 ) Specifically, patients with fibromyalgia typicall y report the presence of at least one comorbid medical or psychiatric condition, including irritable bowel syndrome, migraines, rheumatoid arthritis, bipolar disorder, major depressive disorder, panic disorder and/or agoraphobia, obsessive compulsive disor der, lupus, and chronic insomnia ( Hudson, Goldenberg, Pope, Keck, & Schlesinger, 1992 ; Peres, Young, Kaup Zukerman, & Silberstein, 2001 ; Weir et al., 2006 ) Moreover, fibromyalgia pain symptoms are frequently accompanied by unspecific, physical conditions and complaints, such as cognitive difficulties morning stiffness, painful menstrual periods, headaches, tingling/numbness in hands and feet, and sleep disturbance ( Smith, Harris, & Clauw, 2011 ) Recently, the increased comorbidity of fibromyalgia with sleep disturbance (i.e., 96%), compared to other symptoms, has been recognized by the American College of Rheumatology as evidence d by its rec ent revision of the diagnostic criteria for fibromyalgia to include

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13 severe nonrestorative sleep and fatigue ( Bigatti, Hernandez, Cronan, & Rand, 2008 ; Wolfe et al., 2010 ) Chronic Insomnia Chronic insomnia, a disorder of prolonged sleep disturbance, is another highly prevalent and costly condition that is more commonly seen in comorbid cases. Defined by a t least 6 months of difficulty falling asleep, or staying asleep, and accompanying daytime impairments, chronic insomnia affects approximately 6% of American adults, and estimated annual costs (direct and indirect) exceed $100 billion ( Ancoli Israel & Roth, 1999 ; American Psychiatric Association, DSM IV TR, 2000 ; Fullerton, 2006 ; NIH, 2005 ; Ohayon, 1997 2002 ) Analogous to fib romyalgia, chronic insomnia is a subjective disorder; self reports of daytime impairments and subjective sleep estimates are evaluated to diagnose chronic insomnia. Specifically, negative sleep misperception is a prominent feature of chronic insomnia; ther efore, subjectively reported (i.e., sleep diaries) sleep disturbances are often not confirmed by objective sleep measurements ( i.e., polysomnography, actigraphy; Edinger et al., 2004 ) Moreover, paralleling fibromyalgia, diagnosis of chronic insomnia is more prevalent in populations with chronic disease (37.8%) than the general population ( 8.4%; Ancoli Isr ael, 2006 ) Specifically, conditions with greater risk of comorbid chronic insomnia include: depression, anxiety, hypertension, cancer, heart disease, diabetes, breathing disorders, sleep disordered breathing, urinary disorders, gastrointestinal disorder s, neurologic disorders, as well as chronic pain disorders. Although chronic insomnia is often comorbid with many chronic pain disorders, the comorbidity between fibromyalgia and

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14 chronic insomnia is noteworthy at 75% ( Al Jawder & Bahammam, 2011 ; Ohayon & Roth, 2003 ; Peres et al., 2001 ; Taylor et al., 2007 ) Sleep Disturbances, Changes in Sleep, and Pain The elevated comorbidity of chronic insomnia in patients with fibromyalgia is consistent with current literature, which reveals sleep disturbance s can exacerbate pain and changes in sleep may modulate pain. By definition, sleep disturbances are difficulties of sleep quality or quantity ( Cohen, Menefee, Doghramji, Anderson, & Frank, 2000 ) Overall, sleep disturbance is positively correlated with pain severity ( Morin, Gibson, & Wade, 1998 ; Pilowsky, Crettenden, & Townley, 1985 ; Wilson, Watson, & Currie, 1998 ) Even among healthy individuals, induced sleep disturbance (i.e., sleep deprivation) enhances pain ( Lentz, Landis, Rothermel, & Shaver, 1999 ; Onen, Alloui, Gross, Eschallier, & Dubray, 2001 ) Two common measurements of sleep disturbance include total time spent asleep (TST) and total time awake (TWT). Specifically within populations with chronic disease, afte r controlling for anxiety and depression severity, decrease s in TST predict ed smaller reduction s in pain symptoms and decreases in TWT have been correlated with decreases in pain scores ( Chung & Tso, 2010 ; Edinger, Wohlgemuth, Krystal, & Rice, 2005 ) Further, previous research documents a relationship between sleep difficulties and pain in patients with fibromyalgia. For example, restful sleep is associated with decreased discomfort, and nonrestorative sleep is associated with pain exacerbation in individuals with fibromyalgia ( Affleck, Urrows, Tennen, Higgins, & Abeles, 1996 ; Moldofsky, 1989 ) Moreover, following cognitive behavioral therapy for insomnia in individuals with fibromyalgia, decreases in s leep diary TWT we re associated with decreases in overall pain symptomology ( Roth, Lankford, Bhadra, Whalen, & Resnick, 2012 ) However, although current research

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15 documents the relationship between sleep disturbance and pain in populations with chronic disease, and in fibromyalgia specifically, the underlying cause of the increased likelihood of fibromyalgia and chronic insomnia comorbidity is still unclear. Cognit ive Activation Theory of Stress The Cognitive Activation Theory of Stress (CATS) provides a promising explanation of the increased probability of chronic insomnia diagnosis in patients with fibromyalgia. The CATS posits that normal physiological processes become intolerable at low levels in some individuals, and progress into subjective health complaints. Specifically, susceptible individuals focus increased attention on a normal physiological sensation (i.e., pain, poor sleep). If the sensation continues w ithout explanation or alteration, and high levels of arousal (i.e., physiological, cognitive) are paired with each occurrence, a learned association of helplessness towards the sensation arises. Specifically, prolonged increased levels of stress are associ ated with feelings of helplessness. This sustained psychophysiological response causes sensitization to the stimuli in the central nervous system (CNS), and ultimately dysregulation of the CNS following persistent sensitization. In addition, individuals de velop a cognitive bias for information related to their preoccupation (i.e., cognitive emotional sensitization), and their cognitive processing becomes engrossed in filtering information related to their concerns ( Eriksen & Ursin, 2002 2004 ) CATS, thus, provides a strong theoretical framework to tie the Theories of Chronic Hyperarousal of Insomnia and Central Sensi ti zation in Fibromyalgia together. Both the Hyperarousal Theory of Insomnia and the Theory of Central Sensitization in Fibromyalgia suggest the etiologies of chronic insomnia and fibromyalgia are related to alterations of the CNS. The Hyperar ousal Theory of Insomnia

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16 suggests chronic insomnia is initiated through increased activation of the CNS due to a learned association between negative cognitions/physiological arousal and anxiety from repeated poor sleep occurrence ( Riemann et al., 2010 ) The Theory of Central Sensitization in Fibromyalgia proposes that fibromyalgia is init iated through increased activation of the CNS due to overexcitability of neurons after sustained painful stimulation ( Meeus & Nijs, 200 7 ) Likewise, these similar etiologies may explain the role sleep disturbance plays in pain symptoms. However, pain is also well recognized as a potential causal factor in the initiation of chronic insomnia. For example, within patients with fibromyalgia daily pain is negatively correlated with TST and is positively correlated with TWT ( Roth et al., 2012 ) Therefore, the relationship between sleep and pain may be reciprocal in nature, such that pain interferes with sleep and vice versa. In addition, the CATS suggests that subjective health complaints, such as fibromyalgia and chronic insomnia, share a common pathway in the central nervous system, which may begi n to explain their high comorbidity rate. Previous Neuroimaging Research Currently, brain activity in fibromyalgia and chronic insomnia has been examined in each condition separately, and although previous investigations of brain activity in comorbid condi tions have been performed, the present literature is too sparse to draw definitive conclusions. In patients with fibromyalgia, previous research suggests that areas of the brain related to pain processing (i.e., insula) and the conscious evaluation aspects of cognitive functioning (i.e., posterior cingulate) exhibit increased basal (i.e., without task or stimuli) brain activity ( Harris, 2010 ; Napadow et al., 2010 ) Interestingly, basal brain activity of pain processing areas (i.e., insula) is decreased by supportive therapy ( Napadow, Kim, Clauw, & Harris, 2012 ) Moreover, in patients with chronic

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17 insomnia, previous research suggests disturbed sleep is associated with increased basal brain activity or volume changes of brain regions related to the emotional (i.e., amygdala), somatosensory (i.e., premotor/sensimotor cortex, posterior precuneus) or conscious evaluation (i.e., orbitofrontal cortex) aspects of cognit ive functioning ( Altena, Vrenken, Van Der Werf, van den Heuvel, & Van Someren, 2010 ; Huang et al., 2012 ) Additionally, previous neuroimaging research involving comorbid conditions(i.e., major depressive disorder and social phobia, and bipolar disorder and eating disorder) suggests the presence of two conditions is associated with increased evoked (i.e., pro vided task or stimuli) brain activation of areas related to emotional (i.e., cingulate), somatosensory (i.e., putamen) and conscious evaluation (i.e., putamen) aspects of cognitive functioning ( Hassel et al., 2009 ; Waugh, Hamilton, Chen, Joormann, & Gotlib, 2012 ) However, the effects of sleep disturbance on basal brain activity in patients with comorbid fi bromyalgia and chronic insomnia are still unknown. Present Study The present study examined brain areas associated with greater basal brain activity in individuals with comorbid fibromyalgia and chronic insomnia compared to individuals with fibromyalgia on ly. We predicted that worse sleep (less TST, greater TWT) would predict greater basal activity in brain areas related to emotional response, pain processing, conscious evaluation, and somatosensory aspects of cognitive functioning in individuals with comor bid fibromyalgia and chronic insomnia compared to those with fibromyalgia only.

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18 CHAPTER 2 METHODS Recruitment The present study is a secondary data analysis of a larger study investigating the mechanisms underlying comorbid fibromyalgia and chronic insom nia and the potential of cognitive behavioral treatments for sleep and pain to manipulate those mechanisms For that study, individuals with fibromyalgia completed an extensive baseline screening process that included t wo weeks of sleep diaries to determi ne whether they also met diagnostic criteria for chronic insomnia. The present study included individuals with comorbid fibromyalgia and chronic insomnia (i.e., those who qualified for the parent study) as well as those who met criteria for fibromyalgia, b ut not chronic insomnia (i.e., those who were disqualified from the parent trial) Adult participants were recruited from Gainesville and surrounding areas through radio, newspaper, and television advertisements Criteria for fibromyalgia were consistent with the recommendations of the American College of Rheumatology ( Wolfe et al., 1990 ) Criteria for chronic insomnia were consistent with those of the International Classification of Sleep Disorders 2nd Edition ( AASM, 2005 ) the Diagnostic and Statistical Manual of Mental Disorders Fourth Edition, Text Revision ( American Psychiatric Association. Task Force on DSM IV., 200 0 ) and research diagnostic criteria for chronic insomnia ( Edinger et al., 2004 ; Lichstein, Durrence, Taylor, Bush, & Riedel, 2003 ) Inclusion criteria were : (a) age 18 or above; (b ) individual reports currently suffering from fibromyalgia; (c) fibromyalgia confirmed by tender point test : with application of 4kg force using a dolorimeter participant r eported pain in at least 11 of 18 points, including points in all four body quadrants ( Wagner Force One FDIX Dolorimeter;

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19 Wagner Instruments, Greenwich, CT; Wolfe et al., 1990 ) ; (d) individual reports insomnia (sleep onset or awake time during night > 30 minutes) at least 3 nights per week for more than 6 months; (e) sleep diary confirms insomnia (sleep onset or awake time during night > 30 minutes) at least 6 ni ghts during 2 week baseline period; (f) daytime dysfunction due to insomnia (mood, cognitive, social or occupational impairment); (g) no prescribed or over the counter sleep medication for at least 1 month, or stabilized on medication for at least 6 months ; (h) willing to undergo randomization; and (i) able to read and understand English. Exclusionary criteria were: (a) major psychopathology (e.g., psychotic disorders, substance abuse); (b) a seizure or bipolar disorder; (c) other sleep disorders (e.g., sle ep apnea, periodic limb movements); (d) cognitive impairment based on Mini Mental State Exam ( MMSE, Folstein, Folstein, & McHugh, 1975 ) score lower than 23 ( >9 th grade education) or 19 ( <9th grade education; Almeida, 1998 ) ; (e) suspected sleep disordered breathing based on single night ambulatory monitoring of blood oxygen saturati on and respiration indicating an apnea hypopnea index (AHI) of >15 (Polysomnography; 25 Channel AURA Recording System; G rass Technologies ) All records were scored by a registered polysomnographic technologist and reviewed by a physician board certified in sleep medicine The Project Coordinator conducted initial telephone screening interviews. Doctoral students in American Psychological Association (APA) accredited clinical psychology program conducted clinical interviews u sing structured and semi structured instruments. A licensed clinical psychologist (C. S. M.) certified in behavioral sleep medicine supervised all screening interviews and confirmed final insomnia diagnoses.

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20 Sample Thirty three female participants [mean a ge = 51.24 (SD = 14.90) years] participated in this study (FMI=26, FM=7). The FMI group had a mean age of 53.50 ( SD = 14.05) years ; and 22 were Caucasian, three were African American, and two were of Hispanic origin. Eleven were married and 18 had at leas t some college education. The FM only group had a mean age of 43.57 (16.57) years ; and five were Caucasian and two were African American. Four were married and five had at least some college education. Participants were compensated $100 for their partici pation. The University of 01) approved the study and prior to participation all participants signed informed consent forms. Experimental Materials The neuroimaging p ortion of the study was performed at UF McKni ght Brain Institute, while the remaining portions were co nducted in the UF Sleep Research Laboratory Both sites are located within UF s Health Science Center Complex in Gainesville, FL. Participants underwent a single night of ambulatory polysomnography a nd were instructed to complete a sleep diary each morning for 14 days prior to completing the neuroimaging protocol. For the neuroimaging protocol, a computer controlled Medoc Thermal Sensory Analyzer (Model TSA II; Ramat Yishai, Israel) delivered trains o f 8 suprathreshold heat stimuli via a contact thermode (30 x 30 mm) temperature of 41C, peaked at 49.5C, then returned to baseline with a rise and decline rate o f 10C/second. The duration of each stimulus was approximately 1 second with a 3 second interval separating the peak of each stimulus.

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21 Measures Sleep Diaries Subjective sleep quantity was measured using sleep diaries. The sleep diary ( Lichstein, Riedel, & Means, 1999 ) was completed by each participan t each morning for 14 days ( Appendix). time wake time (i.e., time of last awakening), rise time (i.e., time out of bed for the final time ) nap time Sleep Onset Latency (SOL) amount of time taken to fall asleep Wake after Sleep Onset (WASO) amount of time spent awake after initially falling asleep and before waketime ; and Snooze Time ( SNOOZ ) amount of time from waketime to risetime From the data collected, two sleep variables were derived : (a) total wake time (TWT) computed by adding SOL, WASO, and SNOOZ and (b) total sleep time (TST) computed by subtracting TWT from total time spent in bed (defined as the amount of time between bed time and risetime) Additionally, participants recorded their pain intensity and pain For purposes of the present study, only the following two subjectively measured sleep variables were used: (1) to tal sleep time (TST) and (2) total wake time (TWT). A mean was computed for each variable over the 14 days for each participant. Clinical Pain As part of their sleep diaries (described above), participants provided morning and bedtime ratings of current clinical pain intensity and pain unpleasantness for 14 was instantiated on paper as a 10 centimeter horizontal line with the 2 anchors, and

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22 participants indicated their pain level by marking a spot on the line. To obtain a numerical score for this rating a ruler was used to measure the distance (in centimeters, to the tenth decimal) between the mark and the left end of the line. This value was then multiplied by 10 to rescale it to a 0 to 100 range. The daily values were averaged to get 1 rating of clini cal pain per person. Experimental Paradigm During the neuroimaging protocol participants were comfortably placed on the scanning table in the head first, supine position with their knees supported by a wedge cushion, and feet support by a pillow. Their head positions were then fixed with foam pillows to minimize image artifacts associated with (excessive) head motion. Participants wore both earplugs and earphones for noise protection; the latter also facilitated communication with the participants Durin g the four functional runs in the scanner, participants experienced alternating thermal stimuli presented in 8 pulse trains at .33 Hz by the contact thermode on the ball of the right foot and task negative periods in which the participant did not receive a ny stimuli. Each thermal stimuli period contains three 8 pulse trains. A run consisted of an initial 40 second negative task period, three thermal stimuli that were each 30 seconds in duration separated by 60 second negative task periods, and a final 60 se cond negative task period (Figure 2 1 ). Runs were spaced 120 seconds apart for the aftersensation from the previous thermal stimuli to subside before beginning the next set of thermal stimuli. f MRI Acquisition and Analysis MRI data were acquired with a re search dedicated head scanner using a n 8 Channel Sense head coil (Philips Achieva, 3.0T). The functional images were obtained from a T2 gradient echo planar imaging (EPI) sequence which captured 38 contiguous

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23 transverse slices of the whole brain parallel t o the anterior commissure posterior commissure (AC PC) plane. Additional parameters were: repetition time/echo time (TR/TE) = 2000ms/30ms, flip angle (FA) = 80, field of view (FOV) = 240 x 240, 80mm x 80mm matrix, 3.00mm 3 isotropic voxels with a 0mm slice gap. High resolution 3D anatomical images were acquired using a T1 weighted protocol (180 1 mm axial slices; TR = 2000ms, TE = 4.13ms, FA = 8, matrix = 240 x 240 mm, FOV = 240 mm). The same paradigm was repeated four times for each functional run. Medoc thermal protocol was time locked to the onset of scan acquisition (TR), and each functional run lasted 310 seconds. The first volumes of each run were discarded at the scanner to reduce saturation effects. Functional Data Reduction Data were analyzed with iMac OS X, version 10.6.8. workstation using Brain Voyager (BVQX, Version 2.3 Brain Innovation, Maastricht, the Netherlands; http://brainvoyager.com). Image pre processing rigid body 3D motion correction using trilinear interpolation, slice scan time corr ection with sinc interpolation, spatial smoothing with a 4 mm full width at half maximum (FWHM) Gaussian kernel, voxel wise linear detrending, and high pass temporal filtering to remove non linear drifts below 3Hz. The functional images were co registered to a high resolution 3D anatomic volume and transformed into standard Talairach space ( Talairach & Tournoux, 1988 ) During spatial transformation, functional voxels were interpolated to a resolution of 1mm. Two fixed effects general linear model (GLM) were used to identify cortical regions where TST and TWT significantly predicted the negative task periods, after controlling for thermal stimuli periods as a covariate. Then a group contrast was performed on these brain regions to find those where individuals with FMI exhibited greater brain

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24 activity than individuals with FM. As a precaution against Type I error, resultant statistical parameter maps (SPMs) were thresholded at p < .05, and had a spatial extent of 100 contiguous voxels; th e combination of which established an imagewise p value of .0001 and an effective pixel wise alpha of p < .0001 ( Forman et al., 1995 ) The SPMs were then over laid on a standardized 3D anatomical volume for localization.

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25 Task Negative 40 secs Thermal Stimuli 30 secs Task Negative 60 secs Thermal Stimuli 30 secs Task Negative 60secs Thermal Stimuli 30 secs Task Negative 60secs Scanner Off 120 sec 310 seconds Figure 2 1 Design of the functional runs, the total duration of which lasted 310 seconds.

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26 CHAPTER 3 RESULTS Independence of Sleep Disturbance Indicator s Bivariate correlations of TST and TWT were run to verify independence of the sleep variables. Results revealed a significant, but weak, negative correlation between TST and TWT across groups, r (31) = .41, p < .05, indicating independence in measuring d ifferent aspects of sleep disturbance based on the standard .60 correlation cutoff for independence of variables ( Rubin, 2012 ) Between Group Heterogeneity Independent t tests were run to verify that the sleep variable means of the two groups were significantly different, to ensure group task negative brain activity differences could be attributed to the comorbid insomnia condition. As expected, the groups did significantly differ on sleep as individuals with FMI (M = 403.98, SD = 87.75) had significantly less TST (i.e., slept less during the night on average) than individuals with FM ( M = 459.77, SD = 36.34), t (1) = 2.46, p < .05. In addition, individuals with FMI (M = 122.74, SD = 45.09) had significantly more TWT (i.e., more fragmentation of sleep on average) than individuals with FM ( M = 57.33, SD = 18.80), t (1) = 5.89, p < .001 Bet ween Group Homogeneity Between group homogeneity was tested to verify the groups did not differ on clinical pain to ensure group task negative brain activity differences could be attributed to sleep variables. Results showed that the FMI ( M = 49.47, SD = 1 9.33) and FM only groups ( M = 45.32, SD = 17.31) did not have significantly different clinical pain ratings, t (31) = 0.51, p = .61.

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27 Between group homogeneity was also tested for age, education, race, and marital status to further verify that group task n egative brain activity could be attributed exact tests were run on education, race, and marital status to correct for violation of minimum cell number assumptions and sma ll sample size. d a measure of effect size for test s of mean difference was used to assess the magnitude of the effect for independent t tests d effective size an effect of 0.3 is considered small 0 .5 is medium, and 0 .8 is a large effect ( McGough & Faraone, 2009 ) Cram V a measure of effective size for test s of c ategorical variable association was used to assess the magnitude of the effect for s exact tests. When interpreting V an effect size of 0.00 0.1 0 is interpreted a s a negligible association, 0.10 0.20 as a weak association, 0.20 0.40 as a moderate association, 0.40 0. 60 as a strong association, and 0.80 to 1.00 as a very strong association ( Lea & Parker, 1997 ) Results showed that the two groups were not significantly different in ag e t (31) = 1.57, p = 13, d = .65, education, x 2 (6) = 7.40, p =0.29; FET = 7.09, p = .28 Cram V = .47 race, x 2 (2) = 1.66, p =0.44; FET = 1.58, p = .73 Cram V = .22 or marital status, x 2 (4) = 3.08, p =0.54; FET = 3.31, p = .47 Cram V = .31 Task Negative Brain Activity Group Differences A whole brain GLM analysis examined brain areas associated with greater basal brain activity predicted by TWT and TST in the negative task periods in individuals with FMI compared to individuals with FM only Group comparisons of basal brain activity during the task negative periods revealed significantly greater, t = 4.00, p < .0001, basal brain activity was predicted by TST in the FMI group compared to the FM only group for 9 brain regions: left dorsal poste rior cingulate (BA 31), right inferior temporal gyrus (BA

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28 20; Figure 3 1 ), right medial temporal gyrus (BA 39; Figure 3 2 ), right superior parietal lobule (BA 7), bil ateral precuneus (BA 7; Figure 3 2 ) bilateral superi or frontal gyrus (BA 8; Figure 3 3 ), and left caudate tail ( Table 3 1 ). In addition, during the task negative periods, significantly greater, t = 4.00, p < .0001, basal brain activity was predicted by TWT in the FMI group compared to the FM only group f or 15 brain regions: bilateral cauda te tail, left thalamus, left parahippocampal gyrus (BA19), bilateral inferior frontal g yrus (BA 44; Figure 3 4 right only), bilateral medial temporal gyrus (BA 21; Figure 3 5 right only), right superior temporal gyrus (BA 22; Figure 3 6 ), left inferior p arietal lobule (BA 40), several right medial fr ontal gyri (BA 6, 8, 9; Figure 3 5 ), right occipitotemporalis (BA 37), and left medial globus pallidus ( Table 3 2 for FMI ).

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29 Table 3 1 Coordinates for total sleep time regions with increased activation in the comorbid fibromyalgia and chronic insomnia (FMI) group compared to fibromyalgia only (FM) group Brain Area Number of voxels Coordinates a X Y Z Left caudate tail 106 25 32 16 Left dorsal posterior cingulate BA 31 446 22 46 28 Right inferior temporal gyr us BA 20 287 57 8 17 Left superior frontal gyrus BA 8 149 23 30 46 Right superior frontal gyrus BA 8 171 20 29 46 Right medial temporal gyrus BA 39 510 41 68 18 Right superior partietal lobule BA 7 135 27 68 48 Left, right precuneus BA 7 485 3 6 3 20 Note. a Coordinates of center voxel for significant cluster.

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30 Table 3 2 Coordinates for total wake time regions with increased activation in the FMI group compared to FM only group Brain Area Number of voxels Coordinates a X Y Z Left caudate tail 1088 22 28 22 Right caudate tail 1034 36 32 1 Left thalamus 1232 7 13 21 Left medial globus pallidus 1342 13 7 4 Left parahippocampal gyrus BA 19 599 34 54 1 Left inferior frontal gyrus BA 44 936 49 4 14 Right inferior frontal gyrus BA 44 707 54 1 25 Left medial temporal gyrus BA 21 415 54 50 2 Right medial temporal gyrus BA 21 183 50 38 8 Right superior temporal gyrus BA 22 319 51 3 7 Left inferior parietal lobule BA 40 311 62 37 23 Right medial frontal gyrus BA 6 1142 40 1 45 Right medial frontal gyrus BA 8 2881 27 17 32 Right medial frontal gyrus BA 9 846 34 31 31 Right occipitotemporalis BA 37 678 52 42 7 Note. a Coordinates of center voxel for significant cluster.

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31 Figure 3 1 Increased right in ferior temporal gyrus activation in the FMI group compared to the FM group associated with TST. Figure 3 2 Increased right medial temporal gyrus a nd bilateral precuneus activation in the FMI group compared to the FM group associated with TST A) R ight medial temporal gyrus B) B ilateral precuneus A B

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32 Figure 3 3 Increased l eft and right superior frontal g yri activation in the FMI group compared to the FM group as sociated with TST. A) R ight superior frontal gyrus B) L eft superior frontal gyrus Figure 3 4 Increased right inferior frontal gyrus activation in the FMI group compared to the FM group associated with TWT. A B

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33 Figure 3 5 Increased right superior and medial temporal g yri activation in the FMI group compared to the FM group associated with TWT. A) Right superior temporal gyrus. B) Right medial temporal gyrus. Figure 3 6 Increased right medial frontal gyrus activation in the FMI group compared to the FM group associated with TWT. A B

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34 CHAPTER 4 DISCUSSION The results of th is study suggest that basal brain activation differences occur in individuals with comorbid fibromyalgia and chronic insomnia compared to those with fibromyalgia only. Consistent with our original hypothesis, sleep disturbance, as indicated by decreased average tot al amount of sleep at night and increased average total amount of wake time at night, differentially predicted basal brain activity differences in patients with comorbid fibromyalgia and insomnia compared to those with fibromyalgia. Specifically, decreased average amount of sleep at night was accompanied by increased basal brain activation of primarily emotional response, pain processing, and somatosensory brain areas in individuals with the comorbid disorders when compared to individuals with fibromyalgia only. Also, as hypothesized, increased average amount of time awake at night was accompanied by increased basal brain activation of primarily pain processing and conscious evaluation brain areas in individuals with the comorbid fibromyalgia and chronic ins omnia when compared to individuals with fibromyalgia only. Divergent from the original hypothesis, decreased average amount of sleep at night was not accompanied by increased basal brain activation of primarily conscious evaluation brain areas and increas ed average amount of time awake at night was not accompanied by increased basal brain activation of primarily emotion or somatosensory brain areas in individuals with the comorbid disorders compared to individuals with fibromyalgia only. In addition, incre ased average amount of time awake at night was accompanied by increased basal brain activation of primarily language, planning, and

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35 sleep regulation brain areas in individuals with the comorbid disorders compared to individuals with fibromyalgia only. As many of the brain areas identified are related to conscious evaluation and somatosensory processing, t hese results suggest that sleep problems, or sleep disturbance, such as decreased amount of sleep and increased wakefulness during sleep, may be associate d with catastrophizing (i.e., a form of cognitive bias) and exaggerated somatic focus for intolerable physiological sensations. As catastrophizing and exaggerated somatic focus are typical behaviors noted in individuals with chronic insomnia and fibromyalg ia, and appear to be key components in the CAT S model, it is reasonable that brain regions associated with these cognitive functions would be abnormal in individuals with the comorbid disorders compared to those with fibromyalgia only ( Geisser, Robinson, & Riley, 1999 ; Harvey & Greenall, 2003 ; Mitche ll, Mogg, & Bradley, 2012 ; Vase, Robinson, Verne, & Price, 2003 ) The present study revealed that decreased average amount of sleep at night was accompanied by increased basal brain activation of the posterior cingulate in individuals with the comorbid disorders compared to individuals with fibromyalgia only, analogous to previous research in individuals with comorbid Major Depressive Disorder and social phobia ( Harris, 2010 ; Waugh et al., 2012 ) Furthermore, the present study demonstrated increased average amount of time awake at night was accompanied by increased basal activation of the premotor cortex in individuals with the comorbid disorders when compared to individuals with fibromyalgia only, which is consistent with current chronic insomnia literature ( Huang et al., 2012 ) Moreover, the present study revealed decreased average amount of sleep at night was accompanied by increased

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36 basal brain activation of the bilateral precuneus in individuals with the comorbid disorders compared to individuals with fibromyalgia, similar to the decreased gray matter volume indicated in the posterior precuneus of individuals with chronic insomnia ( Altena et al., 2010 ) The increased basal brain activity noted in the identified regions may suggest an additive effect of increased brain activation in comorbid chronic insomnia. Specifically, separate amounts of increased activati on may be attributed to fibromyalgia and chronic insomnia, such that comorbid chronic insomnia further increases already elevated fibromyalgia related activation of these brain regions. However, whether an additive effect to basal brain activation exists i n comorbid subjective health complaints, such as fibromyalgia and chronic insomnia, is still unknown. Regardless, these results appear to be consistent with the CATS model and our hypothesis that chronic insomnia and fibromyalgia may share a common neurop hysiological pathway. Both of these chronic disorders are associated with negative affect, lack of restorative sleep or rest, and most likely chronic arousal of the central nervous system ( Eriksen & Ursin, 2002 ) After time, these continued symptoms may lead to critical changes in the brain function of the HPA axis and central nervous system, leading to dysregulation of basal brain activity ( Eriksen & Ursin, 2002 ; Wilhelmsen, 2000 ) However, the mea ning of basal brain activity differences in individuals with the comorbid disorders when compared to individuals with fibromyalgia is still unclear. One possible explanation is that the increased basal brain activity of these regions represents an advantag e of comorbid chronic insomnia. Perhaps the brains of individuals with the comorbid disorders become more efficient in localized areas of the

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37 brain, thereby allowing these individuals to cope with the added stress of two comorbid psychophysiological disord ers. However, the reverse explanation, which is consistent with CATS, has greater intuitive appeal. Specifically, the reverse explanation is that the increased basal brain activity of these areas might represent a disadvantage of comorbid chronic insomnia. Perhaps the brains of individuals with the comorbid disorders become less efficient in localized areas of the brain. Specifically, th ose brain areas may become further dysregulated and as a result, more basal brain activation is needed to complete tasks previously requiring less brain activation. The outcomes of this study are significant as they are the first to indicate a predictive relationship between indicators of sleep disturbance and basal brain activity in primarily pain processing, somatosensor y, emotional response, language, planning, and sleep regulation regions. This is the first study to examine basal brain activity not only in the specific context of patients with comorbid fibromyalgia and chronic insomnia, but also in the broader context o f any comorbid psychophysiological disorder. Examining the differences in basal brain activation between individuals with fibromyalgia only and individuals with the comorbid disorders adds much needed information to our knowledge based regarding how stress related chronic disorders develop. Additionally, these results provide support for the hypothesis that similar mechanisms underlie fibromyalgia and chronic insomnia. Perhaps dyregulation due to one chronic disorder predisposes the brain to development of a comorbid chronic disorder. Additionally, as chronic insomnia and fibromyalgia can be treated using cognitive behavioral therapy methods ( Bernardy, Fuber, Ko llner, & Hauser, 2010 ; Espie, Inglis, Tessier, & Harvey, 2001 ; Tang, Goodchild, & Salkovskis, 2012 ) future research is needed to test whether

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38 th e increased brain activation concomitant with comorbid fibromyalgia and chronic insomnia can be corrected by cognitive behavioral therapies. There are a few limitations that need to be acknowledged. First, the sample size was small with unequa l groups, which may have affected the power of the statistical analyses. Specifically, recruitment was indicated for individuals with comorbid fibromyalgia and chronic insomnia. Fibromyalgia only individuals met fibromyalgia criteria and endorsed sleep pro blems, but did not qualify for comorbid chronic insomnia after the 14 day period. Although significant results were still obtained a larger pool of participants with equal group size s may have revealed greater significant results. Second, as the parent st udy examined cognitive behavioral intervention s for pain and insomnia the study may have collected a subset of comorbid individuals that were interested in non medication treatment of FMI, which may affect generalizability of the results to the broader FM I population. Third, task negative periods were fragmented. Instead of continuous resting state data or default mode network scans where f MRI protocols would not include any sensory stimuli or cognitive task, the f MRI scans in the present study alternated between periods of task negative and thermal heat stimulation. Although thermal stimuli and dissipation time were controlled for, task negative periods may not be equivalent to resting state data (i.e., cognitive evaluation of previous painful events, nois e of the scanner, et c. may persist into task negative periods). However, the true impact of this limitation is difficult to estimate as most resting state protocols do not collect participant thought processes during f MRI scans. Thus, this may partially a ttenuate this concern. Fourth, a non comorbid chronic insomnia group was not included in the study as an additional control. Future research should include both a

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39 fibromyalgia only and chronic insomnia only group to further delineate comorbid differences. Fifth, the study included only females, which could affect generalizability of results. However, as both chronic insomnia and fibromyalgia are more prevalent in females, the current study sample appears to be highly generalizable to the FMI population ( Johnson, Roth, Schultz, & Breslau, 2006 ; Lichstein, 2004 ) The present study will be extended to inve stigate whether additive effects of identified brain areas exist in individuals with FMI when compared to individuals with FM, as a possible developmental mechanism for increased FMI comorbidity. Additionally, future work will examine neural changes in pat ients with FMI follow ing cognitive behavioral therapies for pain and insomnia This will begin to elucidate possible mechanisms (i.e., biological, physiological) of cognitive behavior al effectiveness and durability in individuals with FMI. For e xample, p erhaps increased basal brain activity is corrected (i.e., decreased) by cognitive behavioral therapy for insomnia. Furthermore, if basal brain activity is decreased, these reductions should be qualified to clarify if the basal brain activation d ecreases found in individuals with FMI are equivalent or below levels noted in individuals with FM. Also, future investigations should replicate the present results in continuous resting state data to more closely parallel previous studies of resting state and default mode network research in chronic insomnia and fibromyalgia. Moreover, it is important for prospective studies to examine basal brain activity differences in individuals with fibromyalgia only and chronic insomnia only in comparison to individu als with the comorbid disorders.

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40 APPENDIX SLEEP DIARY ID _______________ Date____________ B_ T__ P F__: W__ This Diary is designed to gather information about your night of sleep, and the activity the takes place prior to that n ight of sleep. You will fill the top po r tion out before going to bed, and the bottom portion when you wake up in the morning. Please remember to press the event marker on your Actiwatch when you get into bed at night and when you get out of bed in the morn ing. EVENING: Please fill this section out right before you go to bed on_____________________ I had ____________ alcoholic drinks today. I had ____________ caffeine drinks today. I smoked ____________cigarettes/cigars today. Removed Watch Time off Time On Reason If additional space is needed, please write on the back of this page Please mark on the following two lines how you currently feel. 0 _______________________________________________100 no pain most intense pain sensation sensation imaginable 0 _______________________________________________100 not at all most unpleasant unpleasant imaginable ************************************************************************** ***** NEXT MORNING: Please fill this section out the morning of __________________________ 1. I napped for ____________ minutes yesterday. 2. I napped ______ times yesterday. 3. I napped in the ___morning ___afternoon ____evening (check all that appl y) 4. I went to bed last night at ____________ AM/PM. 5. It took me ____________ minutes to fall asleep. 6. I woke up ____________ times last night. 7. I was awake for ____________ minutes in the middle of the night. 8. My final wake up time was ____ ________ AM/PM. 9. I got out of bed at ____________ AM/PM. Bedtime Medications (List name, time, & dose) Pain Medications (List name, time, & dose)

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41 10. I would rate my quality of sleep last night as ________. 1. very poor 2. poor 3. fair 4. good 5. excellent Please mark on the following two lines how you currently feel. 0 __________________ _____________________________100 no pain most intense pain sensation sensation imaginable 0 __________ _____________________________________100 not at all most unpleasant unpleasant imaginable

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48 BIOGRAPHICAL SKETCH Karlyn Vatthauer was born and raised in Texas. Prior to her current position as a she attended the University of North Texas as an undergraduate student, where she majored in Psycholog y, minored in Biology, and conducted research in the UNT Insomnia Research Laboratory. Subsequently, she worked as a research assistant at the University of Florida for one year in the UF Sleep Research Laboratory and the UF Pain and Behavioral Health Rese arch Center investigating the relationship between sleep and cognitive functioning variability in older adults. She aspires to work in a clinical and academic medical setting, predominantly performing research in sleep and cognitive functioning and providing clinical services to individuals with sleep difficulties.