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The Effect of Motor Symptom Onset Laterality on Facial Expressivity in Parkinson's Disease

Permanent Link: http://ufdc.ufl.edu/UFE0022026/00001

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Title: The Effect of Motor Symptom Onset Laterality on Facial Expressivity in Parkinson's Disease
Physical Description: 1 online resource (61 p.)
Language: english
Publisher: University of Florida
Place of Publication: Gainesville, Fla.
Publication Date: 2008

Subjects

Subjects / Keywords: disease, expressivity, facial, laterality, parkinson
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: The purpose of the present study was to examine the effect of motor symptom laterality commonly found in Parkinson's disease (PD) as well as mood and motor symptoms on different aspects of facial expressivity. Most patients with PD initially present with lateralized motor symptoms on one side of the body, left or right. This asymmetry usually persists throughout the course of the disease and reflects differential disruption of contralateral basal ganglia-frontal lobe dopaminergic systems. While a growing number of studies have reported that laterality of symptom onset may also influence non-motor symptoms of the disease (i.e., cognition), it remains unknown whether emotional processing is affected by symptom onset laterality. A cardinal symptom of PD is a 'masked face,' or significantly diminished facial expressivity. Based on views regarding a right hemispheric specialization for emotional behavior, we hypothesized that patients with left-sided motor symptom onset (implicating greater right hemisphere involvement) would display greater impairments in facial expressivity than those with right sided symptom onset. We also predicted that mood and PD-specific motor symptoms would contribute to diminished facial expressivity. Twenty six patients with idiopathic PD (13 left symptom onset, 13 right onset) and 13 healthy controls were videotaped while posing facial expressions of fear, anger, and happiness. Facial expressions were digitized and analyzed using custom software that extracted 5 variables: 2 measures of dynamic movement change (total and peak entropy), and 3 temporal variables (initiation time, rise time, duration). Self-report measures of depression (Beck Depression Inventory-II) and apathy (Apathy Evaluation Scale) were also given. Repeated measures ANOVAs and linear regressions were used to analyze the data. Bonferroni-corrected post-hoc analyses revealed that the left-onset PD patients were significantly slower in initiating facial expressions than were right-onset PD patients or controls, regardless of expression posed F (2,36) = 8.21, p < .05. The groups did not significantly differ in terms of the entropy variables or other temporal variables. Furthermore, mood (i.e., depression or apathy) and disease-specific factors (i.e., symptom type) were unrelated to facial expressivity. These results suggest an effect of motor symptom asymmetry on initiation of facial expressions among patients with PD. The findings are more in line with views that emphasize the role of the right hemisphere on attentional and intentional behavior, rather than 'emotion,' per se. In other words, slower initiation times for posed facial expressions among PD patients with greater right cortical-subcortical dysfunction may reflect reduced ability to initiate and respond rather than defective emotional processing as initially proposed. Overall, these findings highlight the potential importance of symptom laterality in non-motor aspects of Parkinson's disease.
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.
Thesis: Thesis (M.S.)--University of Florida, 2008.
Local: Adviser: Bowers, Dawn.
Electronic Access: RESTRICTED TO UF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE UNTIL 2009-05-31

Record Information

Source Institution: UFRGP
Rights Management: Applicable rights reserved.
Classification: lcc - LD1780 2008
System ID: UFE0022026:00001

Permanent Link: http://ufdc.ufl.edu/UFE0022026/00001

Material Information

Title: The Effect of Motor Symptom Onset Laterality on Facial Expressivity in Parkinson's Disease
Physical Description: 1 online resource (61 p.)
Language: english
Publisher: University of Florida
Place of Publication: Gainesville, Fla.
Publication Date: 2008

Subjects

Subjects / Keywords: disease, expressivity, facial, laterality, parkinson
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: The purpose of the present study was to examine the effect of motor symptom laterality commonly found in Parkinson's disease (PD) as well as mood and motor symptoms on different aspects of facial expressivity. Most patients with PD initially present with lateralized motor symptoms on one side of the body, left or right. This asymmetry usually persists throughout the course of the disease and reflects differential disruption of contralateral basal ganglia-frontal lobe dopaminergic systems. While a growing number of studies have reported that laterality of symptom onset may also influence non-motor symptoms of the disease (i.e., cognition), it remains unknown whether emotional processing is affected by symptom onset laterality. A cardinal symptom of PD is a 'masked face,' or significantly diminished facial expressivity. Based on views regarding a right hemispheric specialization for emotional behavior, we hypothesized that patients with left-sided motor symptom onset (implicating greater right hemisphere involvement) would display greater impairments in facial expressivity than those with right sided symptom onset. We also predicted that mood and PD-specific motor symptoms would contribute to diminished facial expressivity. Twenty six patients with idiopathic PD (13 left symptom onset, 13 right onset) and 13 healthy controls were videotaped while posing facial expressions of fear, anger, and happiness. Facial expressions were digitized and analyzed using custom software that extracted 5 variables: 2 measures of dynamic movement change (total and peak entropy), and 3 temporal variables (initiation time, rise time, duration). Self-report measures of depression (Beck Depression Inventory-II) and apathy (Apathy Evaluation Scale) were also given. Repeated measures ANOVAs and linear regressions were used to analyze the data. Bonferroni-corrected post-hoc analyses revealed that the left-onset PD patients were significantly slower in initiating facial expressions than were right-onset PD patients or controls, regardless of expression posed F (2,36) = 8.21, p < .05. The groups did not significantly differ in terms of the entropy variables or other temporal variables. Furthermore, mood (i.e., depression or apathy) and disease-specific factors (i.e., symptom type) were unrelated to facial expressivity. These results suggest an effect of motor symptom asymmetry on initiation of facial expressions among patients with PD. The findings are more in line with views that emphasize the role of the right hemisphere on attentional and intentional behavior, rather than 'emotion,' per se. In other words, slower initiation times for posed facial expressions among PD patients with greater right cortical-subcortical dysfunction may reflect reduced ability to initiate and respond rather than defective emotional processing as initially proposed. Overall, these findings highlight the potential importance of symptom laterality in non-motor aspects of Parkinson's disease.
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.
Thesis: Thesis (M.S.)--University of Florida, 2008.
Local: Adviser: Bowers, Dawn.
Electronic Access: RESTRICTED TO UF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE UNTIL 2009-05-31

Record Information

Source Institution: UFRGP
Rights Management: Applicable rights reserved.
Classification: lcc - LD1780 2008
System ID: UFE0022026:00001


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THE EFFECT OF MOTOR SYMPTO M ONSET LATERALITY ON FACIAL EXPRESSIVITY IN PARKINSONS DISEASE By ANNE NOELLE NISENZON A THESIS PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLOR IDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE UNIVERSITY OF FLORIDA 2008 1

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2008 Anne Noelle Nisenzon 2

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To my family. 3

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ACKNOWLEDGMENTS First, I sincerely thank my mentor, Dr. Dawn Bowers, for her endless patience, care, encouragement, and support. I also thank my colleagues in the Cognitive Neuroscience Laboratory for their kind and helpful advice. I would like to thank my defense panel, Drs. Bowers, Perlstein, Perri, and Wiens, for their time in reviewing this study and providing valuable suggestions. Finally, I thank my parents, Alex and Irina Nisenzon, for their support in my professional endeavors. 4

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TABLE OF CONTENTS page ACKNOWLEDGMENTS...............................................................................................................4 LIST OF TABLES................................................................................................................. ..........7 LIST OF FIGURES.........................................................................................................................8 ABSTRACT.....................................................................................................................................9 CHAPTER 1 INTRODUCTION................................................................................................................. .11 Parkinsons Disease: Symp tomatology and Neuropathology.................................................12 Lateralization of Em otional Processing..................................................................................15 Emotion in Parkinsons Disease.............................................................................................17 Facial Expressivity and Parkinsons Disease.........................................................................18 2 STATEMENT OF THE PROBLEM......................................................................................21 3 METHODS...................................................................................................................... .......25 Participants.............................................................................................................................25 Measures.................................................................................................................................28 Procedures..................................................................................................................... ..........29 Statistical Analyses........................................................................................................... ......32 4 RESULTS...................................................................................................................... .........34 The Effect of Laterality on Facial Expressivity......................................................................34 Mood and Motor Correlates of Expressivity..........................................................................37 Relationship between Mood and Facial Expressivity.....................................................37 The Relationship between Motor Symptoms and Expressivity......................................39 5 DISCUSSION................................................................................................................... ......41 Summary and Interpretation of the Findings..........................................................................41 Latency to Expression as an Action-Intentional Deficit.........................................................44 Limitation of the Present Study..............................................................................................46 Directions for Future Research...............................................................................................49 Conclusion..............................................................................................................................50 APPENDIX DESCRIPTIVE STATISTICS AND ANOVA TABLES FOR PRIMARY AIM..................52 5

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LIST OF REFERENCES...............................................................................................................54 BIOGRAPHICAL SKETCH.........................................................................................................60 6

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LIST OF TABLES Table page 3-1. Participant Demographics............................................................................................ 27 4-1. Descriptive Statistics for Mood and Motor Variables..................................................37 4-2: Linear Regression Analysis of Mood Variables on Facial Expressivity......................39 4-3: Linear Regression Analysis of Motor Variables on Facial Expressivity.....................40 A-1. Descriptive Statis tics for Entropy Variables...............................................................52 A-2. ANOVA Summary : Entropy Variables.......................................................................52 A-3. Descriptive Statisti cs for Temporal Variables.............................................................53 A-4. ANOVA Summary: Temporal Variables....................................................................53 7

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LIST OF FIGURES Figure page 1-1. Simplified pathophysiological model of motor and emotional dysfunction in Parkinsons disease............................................................................................................ 14 3-1. Digitizing the Moving Face..............................................................................................3 2 3-2. Entropy Curve....................................................................................................................33 4-1. Bar Graph: Latency to Initiate Facial Expressions............................................................36 8

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Abstract of Thesis Presen ted to the Graduate School of the University of Florida in Partial Fulfillment of the Requirements for the Degree of Master of Science THE EFFECT OF MOTOR SYMPTO M ONSET LATERALITY ON FACIAL EXPRESSIVITY IN PARKINSONS DISEASE By Anne Noelle Nisenzon May 2008 Chair: Dawn Bowers Major: Psychology--Clinical and Health Psychology The purpose of the present study was to examin e the effect of moto r symptom laterality commonly found in Parkinsons disease (PD) as well as mood and motor symptoms on different aspects of facial expressivity. Most patients with PD initially present with lateralized motor symptoms on one side of the body, left or right. This asymmetry usually pers ists throughout the course of the disease and reflects differential disruption of contralateral basal ganglia-frontal lobe dopaminergic systems. While a growing number of studies have reported that lateral ity of symptom onset may also influence non-motor symptoms of the diseas e (i.e., cognition), it remains unknown whether emotional processing is affected by symptom onset laterality. A cardina l symptom of PD is a masked face, or significantly diminished facial expressivity. Based on views regarding a right hemispheric specialization for emotional behavior we hypothesized that pa tients with left-sided motor symptom onset (implicating greater right hemisphere involvement) would display greater impairments in facial expressivity than those with right sided symptom onset. We also predicted that mood and PD-specific motor symptoms would cont ribute to diminished facial expressivity. Twenty six patients with idiopathic PD (13 left symptom onset, 13 right onset) and 13 healthy controls were videotaped while posing f acial expressions of fear, anger, and happiness. 9

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10 Facial expressions were digitized and analyzed using custom software that extracted 5 variables: 2 measures of dynamic movement change (total and peak entropy), and 3 temporal variables (initiation time, rise time, duration). Self-report measures of depression (Beck Depression Inventory-II) and apathy (Apat hy Evaluation Scale) were also given. Repeated measures ANOVAs and linear regressions were used to analyze the data. Bonferroni-corrected post-hoc analyses revealed that the le ft-onset PD patients were significantly slower in initiating fa cial expressions than were right -onset PD patients or controls, regardless of expression posed [F (2,36) = 8.21, p <.05]. The groups did not significantly differ in terms of the entropy variables or other te mporal variables. Furthermore, mood (i.e., depression or apathy) and disease-specific factors (i.e., symptom type) were unrelated to facial expressivity. These results suggest an eff ect of motor symptom asymme try on initiation of facial expressions among patients with PD. The findings are more in line with views that emphasize the role of the right hemisphere on attentional and in tentional behavior, rather than emotion, per se. In other words, slower initiation times for posed facial expr essions among PD patients with greater right cortical-subc ortical dysfunction may reflect re duced ability to initiate and respond rather than defective emo tional processing as initially pr oposed. Overall, these findings highlight the potential importanc e of symptom laterality in no n-motor aspects of Parkinsons disease.

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CHAPTER 1 INTRODUCTION Parkinsons disease (PD) is a neurodegenerative movement disorder that arises from dopamine loss in deep brain structures and l eads to widespread functional impairment. Prevalence reports estimate approximately one million people in the United States with the disease, with incidence reports of up to 60,000 new cases diagnosed each year (McDonald, Richard, and Delong, 2003). Idiopathic PD is comm only diagnosed after the age of 60, and has a gradual, insidious, and often lateralized onset of motor symptoms which worsen with disease progression. While pharmacological and surgical interventions are available to alleviate symptoms temporarily, there is no known cure to reverse or prevent further degeneration. An often overlooked yet important symptom of Parkinsons disease is a masked face. This term refers to the mannequin-like expressi onless face that is characteristic of most individuals with PD. Due to th eir reduced propensity to facia lly convey either positive or negative emotions, PD patients are often misdiagnos ed as being depressed or apathetic. While both these mood states commonly occur in PD, their rates may be inflated due to misperception by healthcare providers. As such, it is important to parcel out the effects of diminished facial expressivity from that of true mood disturbance. Relative to other neurodegenerative disorders, asymmetric symptom onset is a notably unique feature of PD and reflects greater pathology in contralateral s ubcortical regions. Hemispheric laterality is also well-documented in emotional research, and different theories speculate on how the right and left cortical hemispheres process a wide array of emotionallycharged information. These views on hemispheric differences in emotional behavior are relevant to Parkinsons disease because s ubcortical regions affected in th e disorder directly project to cortical regions on the same side of the brai n. Thus, laterality of motor symptom onset may 11

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potentially play an important role in the occu rrence of the masked face and emotional symptoms in Parkinsons disease. The primary goal of the current study was to compare emotional facial expressivity in right-sided onset and left-sid ed onset (indicating greater left or right neuropathology, respectively) PD patients. To do so, we used novel computer imaging techniques for calculating dynamic movement changes over the face (i.e., entropy) as opposed to the more traditional subjective judgments used in prev ious research. Additionally, the effects of m ood and PD motor symptoms on facial expressivity were examin ed. Before discussing the specific hypotheses, a brief review of literature will now be presented pertaining to: 1) Parkinsons disease symptomatology and its neuropathol ogical correlates, 2) theories of hemispheric dominance in emotional behavior, 3) emotion a nd facial expressivity in PD. Parkinsons Disease: Symptomatology and Neuropathology Parkinsons disease is diagnosed based upon the presence of four cardinal motor symptoms: bradykinesia, rigidity, tremor, and postural instability. Bradykinesia refers to an overall slowing of movement, and can be witnesse d by asking patients to ra pidly tap their fingers at a given amplitude. Bradykinesia is a distinct ive feature of PD and must be observable for affirmative diagnosis. Rigidity refers to muscle stiffness and is characterized by resistance to passive movement of a limb. Tremor in PD involves involuntary shaking of the limb and typically occurs as a resting tremor, which su bsides when the person engages in a purposeful movement. Other features of Parkinsons disease include postural instability or poor balance, and gait disturbances, in which patients walk wi th a stooped posture and take small, quickened steps. Patients may be classified as tremor predominant or rigid/akin etic type depending on which symptoms are most evident during a motor examination. Additional hallmark features of PD are slurred speech, small cramped writing, and diminished facial expressivity. 12

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In terms of pathophysiology, Park insons disease essentially originates from the disrupted functioning of the basal ganglia, a midbrain structure composed of the striatum, globus pallidus (GP), subthalamic nucleus (STN), and the substan tia nigra. These nuclei operate together to modulate functioning of higher cortic al areas via the thalamus. In Parkinsons disease, neurons in the substantia nigra pars compacta (SNc ) stop producing dopamine, thereby disrupting connectivity in various parallel closed-loop basal ganglia-thalamo -cortical circuits that are topographically organized and f unctionally specialized. Alexa nder, DeLong, & Strick (1986) identified 5 such circuits, each influencing mo tor, cognitive, or emotional functioning (see Figure 1-1 for motor and limbic circuitry). By the time initial motor symptoms are experienced in PD, the SNc is approximately 70% inactive (Obeso et al., 2002). In early stages of Parkinson di sease, behavioral symptoms are most often lateralized to one side of the body. With further progression, how ever, these symptoms appear bilaterally, but usually remain worse on the presenting side (Lee et al., 1995). Imag ing studies and postmortem cell counts suggest greater neuronal loss in the substantia nigra contralateral, or opposite, the initially more affected body side (K empster et al., 1989). It is currently unknown whether asymmetrical neurodegene ration is due to inborn variati ons in dopaminergic neurons, differential vulnerability to the disease, or by random occurrence (Dja ldetti, Ziv, & Melamed, 2006). The neuropathology associated with specific mo tor symptoms in PD has been elucidated through neuroimaging studies. Positron emi ssion tomography (PET) studies show that bradykinesia and rigidity both arise from excessive inhibition of the thalamus and subsequent motor cortices due to excitatory glutaminergic projections on the internal globus pallidus (Lozza et al., 2002). The disease mechanism of tremor is not as clear, though some researchers postulate 13

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that it involves hypo activation of the basal ga nglia along with hyperactiva tion of brain structures outside the basal ganglia-thalamo-c ortical loops, specifically in th e cerebellum (Antonini et al., 1998; Yu et al., 2007). Thus, loss of nigral dopaminergic cells le ads to a gross imbalance of chemical signals which results in motor impa irment and, ultimately, cognitive and emotional deficits. Medications (levodopa and dopamine agonists) and su rgical interventions, including deep brain stimulation (DBS) and damaging hypera ctive areas of the basal ganglia or thalamus, have been successfully employed to quell motor symptoms by temporarily reestablishing neurochemical balance. However, neither medicati on nor surgical approaches are able to stop or reverse neurodegeneration associated with Parkinsons disease. Motor Circuit Limbic Circuit Motor Cortex Putamen Lateral Pallidum Thalamus (medial dorsal nucleus) + + Anterior Cingular Cortex Ventral Striatum Ventral Pallidum Thalamus (dorsolateral nucleus) + SNc + + Figure 1-1: Simplified pathophys iological model of motor a nd emotional dysfunction in Parkinsons disease. Dopaminergic cells in the substantia nigra pars compacta die, leading to an imbalance of excitatory and inhibitory signals passed from higher cortical structures to the striatum via the thalamus. There are 5 segregated parallel basal ganglia loops, each of which involve di fferent cortical and s ubcortical structures and modulate different areas of functioning. Illustrated here are the motor and limbic circuits, influencing physical and emotional functioning, respectively. 14

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Lateralization of Emotional Processing The limbic system has long been viewed as the primary neuroanatomic substrate for emotion (Papez, 1995). It includes several key structures (amygdala, hypothalamus, septum, cingulate, nucleus accumbens) that have been li nked to appetitive/reward and avoidance/attack behaviors. Basal ganglia systems that overlap with limbic circuitry (i.e., nucleus accumbens, amygdale, cingulate) have also been implicated in emotion. Specifically, neuroimaging studies have revealed activation in the medial prefront al cortex and anterior cingulate during general emotional processing, regardless of emotion el icited or induction met hod (Phan et al., 2002). These particular regions are part of a basal ganglia circuit known as the limbic loop, and are impacted by the subcortical dysfunction as seen in PD. While involvement of the limbic system and basal ganglia modulation is apparent in emotional behavior, the role of the cortical he mispheres has long been debated. One overarching view is that cortical regions serve to provide higher order modulation of underlying limbic regions. What is less clear is how the two hemis pheres play differential roles in this cortical modulation. There are two competing theories as to how emotion is processed in higher cortical areas the right hemisphere model and the bivalent model. According to the right hemisphere model, the right cortical hemisphere is dominan t for mediating all emotio nal behavior, regardless of affect. This view is suppor ted by lesion studies that demonstrate damage to the right versus left hemisphere leads to significant deficits in th e perception and expression of emotional stimuli including facial expressions, em otional prosody, and lexical aff ective expression and experience (Borod, 1992; Borod et al., 1998; Bowers, Baue r, & Heilman, 1993; Heilman & Bowers, 1990; Liotti and Tucker, 1995). Similarly, patients wi th right hemisphere lesions show greater impairment in recognizing faci al expressions of emotion or emotional prosody (Bowers et al., 1985; Bowers et al., 1987). Regarding emotiona l experience, a neuroimaging study of apathetic 15

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stroke patients revealed greater hyperintensities in the right front o-subcortical pathway than in the left, despite stroke severity (Brodaty et al., 2005). Furthe rmore, studies conducted on facial expressivity have shown that norm al adults express their emotions more intensely on the left side of the face, which is contralate rally controlled by the right hemi sphere, and that patients with right hemisphere damage are less facially expr essive in general (Borod and Caron, 1980; Borod, 1992). In terms of potential mechanisms underlying the right hemisphere hypothesis of emotion, some have speculated that the functional organiza tion of the right hemisphere has made it more suitable for emotional processing. The right hemi sphere has been shown to be specialized in integration and representation of information, which is necessary in nonverbal emotional communication. This explanation of right he misphere dominance in emotion stems from findings that focal left hemisphere lesions result in discrete cognitive deficits whereas focal damage in the right hemisphere produce diffuse deficits in several domains (Semmes, 1968). Thus, the right hemisphere may be crucial in th e cognitive mediation of emotional experience (Liotti & Tucker, 1995). Another line of evidence suggests great er connection density between regions in the right hemisphere, which may result in more varied communication pathways with the limbic system (Tucker, 1991). Moreover, a recent study featuring diffusion tensor tractography confirmed asymmetrical white matte r organization in the br ain (Barrick et al., 2006). Another view as to hemispheric laterality of emotional processing is the bivalent hypothesis. According to this hypothesis, the righ t hemisphere is more specialized in processing negatively-valenced emotions while the left he misphere is more active in positive emotions. Historically, this view derived from observati ons of differing emotional changes experienced by 16

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patients who suffered strokes of the left or ri ght hemisphere. Goldst ein (1939) noted that individuals with left hemisphere strokes had ca tastrophic reactions, whereas those with right hemisphere strokes were emotionally flattene d and apathetic. Furthermore, post-stroke depression following left hemisphere strokes has been shown to be particularly severe when subcortical regions were invol ved (Starkstein, Robinson, & Pr ice, 1987). These clinical findings, in conjunction with subs equent research on mood-relate d EEG asymmetries in normals (Davidson, 1995) led to the hypothesis that bot h hemispheres were involved in emotional processing, though each differed in the specific type of emotions, i.e., positive versus negative. Although intriguing, the bivalent mo del has not been consistently supported in empirical studies of emotional perception or produc tion (Borod, 2000; Heilman et al., 2003). Moreover, there has been minimal support for the view that the left hemisphere mediates positive emotions (see Harciarek et al., 2006). In summary, two major models have been proposed regarding the role of the two hemispheres in mediating emotional behavior. In one model, the right hemisphere takes on primary responsibility for medi ating all aspects of emotiona l behavior including perception, expression, and experience. In the second (bival ent) model, the left hemisphere mediates pleasant/approach related emoti ons whereas the right hemis phere is more involved in negative/avoidance related emotions. Emotion in Parkinsons Disease Emotional behavior is often researched in Park insons disease as mood disorders are highly comorbid with the disease. Depressi on is commonly observed with prevalence rates ranging from 4% to 70% among patients (Cubo et al., 2002). The basis for depression in Parkinsons disease is unknown, although it involves both biologica l and psychological factors. Psychological factors include reacti ons to receiving a diagnosis of a neurodegenerative illness, 17

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difficulties in adjusting to lifestyle changes, and alterations in family dynamics and spousal roles. Biologically, dopamine loss in the limbic circuit of the basal ga nglia as well as disruption of serotonin and other neurotransmitter systems are considered key components in PD-related depression (Lieberman, 2006). While antidepressants such as SSRIs are often prescribed in this population to treat depression, there is a lack of evidence for antidepressant efficacy among PD patients (Weintraub et al., 2003). Another common mood disorder in Parkinson disease is apathy, which is a relatively new area of research in this populati on. Apathy refers to a loss of mo tivation in affective, cognitive, and behavioral domains (Marin, 1991). Symp toms of apathy have traditionally been misdiagnosed as being symptoms of depression, thereby possibly inflating its rates. The depressive symptom of anhedonia, or loss of interest, is especially similar to the characteristic features of apathy. However, the two are dissoc iable in PD patients according to the KirschDarrow et al. (2006) finding that apathy can occur in the absence of depres sion and vice versa. The neurobiological substrates of apathy are unknown although apat hy has been associated with dysfunction in mesial frontal and anterior cingulate regions (f or review, see Levy & Dubois, 2006). Facial Expressivity and Parkinsons Disease Emotional facial expressivity is a funda mental form of communication, and, when impaired as it often is in Parkinsons disease, can have far-reaching conse quences in the patients quality of life and interpersona l relationships. For example, the seemingly ubiquitous symptom of depression among PD patients may be overd iagnosed due to misattribution of negative emotional states by healthcare workers (Pentland et al., 1988). Additionally, diminished facial expressivity can impair communi cation between patients and love d ones, leading to confusion 18

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and frustration on both ends. Paying greater atte ntion to this debilita ting yet underrepresented symptom of PD may ultimately open the doors for more comprehensive treatment options. Thus, it is important to understand the mechanical aspects of facial expressivity and how it is disrupted in Parkinsons disease. Greater elucidation of the process of diminished facial expressivity may lead to better research techniques, and, ultimately, more comprehensive treatment options. Facial expressions are created through projections from the motor cortex to the brain stem via the corticobulbar system, a white matter path way which controls the muscles of the face, head, and neck. Corticobulbar projections to cell body groups controlling movements in the lower face come exclusively from the contralateral hemisphere while bilateral projections stimulate the upper face (Rinn, 1984). This system describes production of posed or voluntary expressions that do not involve emotionality. Spontaneous emotional ex pressivity is more subcortically modulated and was originally thou ght to involve only an extrapyramidal motor system separate from the corticobulbar pathway. The extrapyramidal system, which includes the basal ganglia and the nigrostriatal pathway, modulates motor activity without directly innervating motor neurons (Rinn, 1984). More recent research states that both the corticobulbar and extrapyramidal systems are implemented to create fluid, effective posed and spontaneous facial expressions (Simons et al., 2004). The mechanism underlying diminished facial expressivity in Parkinsons disease is not fully understood. One view indicates that dopamine depletion in the basal ganglia disrupts healthy functioning of the extrapyramidal pa thway, thereby greatly affecting spontaneous expressivity (Turner et al., 2003; Rinn, 1984). However, Bowers et al. (2006) demonstrated that voluntary expressions are also diminished in PD patients, as impairment in frontostriatal circuitry may have a dampening effect on expression intensity, regardless of intention. Another view 19

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20 speculates that depressive symptoms may lead to reduced emotional expressivity, although nondepressed patients also present with masked faces. Thus, diminished facial expressivity is not simply a result of affective dysfunction (McD onald et al., 2003; Bowers et al., 2006). Furthermore, Bowers et al. (2006) found that PD patients were less expressive than healthy controls regardless of emotional valence (i.e., ha ppy vs. sad). The loss of muscle tone in the face resulting from overall motoric disability in PD may also cause problems in facial expressivity (De Letter et al., 2003). In sum, speculations as to the physical and emotional substrates of the masked face in PD have been inconclusive, reflec ting the elusive nature of this symptom and the relative dearth of research conducted in this area.

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CHAPTER 2 STATEMENT OF THE PROBLEM Although Parkinsons disease (PD) is classically considered a motor disorder, it is now viewed as a multi-modal disorder affecting mo tor, cognitive, and emotional processing. However, there are still many unanswered questions regarding patients behavioral functioning. One such question relates to the importance or relevance of motor symptom onset asymmetry. While motor asymmetry clearly reflects disruptio n of subcortical-frontal dopaminergic systems on one side of the brain, the i ssue becomes whether this neuropathological asymmetry has any consequences for non-motor behaviors (i.e., cognitive or emotional). Neuropsychological research of motor symptom onset asymmetry in Parkinsons disease has primarily focused on the impact of laterali ty on cognitive impairment. This comes as no surprise given that lateralized br ain damage is often associated w ith material specific deficits, depending on whether the left (verbal) or right (visuospatial) hemisphere is affected. Historically, inferences about laterality of function were based on studies of patients with focal cortical lesions (Geschwind, 1979). Over time, observations of material-specific cognitive deficits were also described in patients with lateralized subcortical dama ge (i.e., thalamus) (Stuss et al., 1988). The basis for these subcortical laterality effects wa s unclear, as they could reflect intrinsic right-left processing differences by subc ortical regions and/or di srupted projections to cortical regions via dysfuncti onal subcortical pathways. Re gardless of the underlying mechanism, several studies with Parkinsons di sease patients have s hown that right sided symptoms (indicating greater left hemisphere dysfunction) were associated with verbal deficits whereas left sided symptoms were associated with spatial deficits. Such findings indicate a clear double dissociation of impairment based on latera lized cognitive abilities (Amick et al., 2006; Blonder et al., 1989a). Double dissociation is the strongest level of inference in 21

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neuropsychology and behavioral neurology (Teuber, 1955), thus providing substantial weight to these findings. However, it should be noted that not all studies ha ve found a significant association between latera lity and various cognitive deficits in patients with PD, and, thereby, continues to call into question th e importance of laterality (Cubo et al, 2000; St. Clair et al., 1998). In contrast to cognitive st udies, the relationship between motor asymmetry and emotional symptoms in PD has largely gone untouched. This hole in the literature is quite remarkable given that there are dozens of replicated st udies showing hemisphe ric specialization in processing emotion as well as separate stud ies conducted on emotional behavior in PD. Although several studies have focused on the effect of asymmetrical symptomatology on depression in PD and yielded inc onclusive and conflicting results (F leminger, 1991; Spicer et al., 1988; Starkstein et al., 1992), minima l attention has been paid to faci al expressivity in relation to laterality of symptom onset. Thus, the overall goal of the present study was to examine the influence of motor symptom laterality in Parkinsons disease on differe nt aspects of emotional behavior, particularly facial expressivity and mood. Th e underlying basis for such an e ndeavor derives from two lines of evidence: a) the tightly c oupled functional relationship betw een subcortical regions within each hemisphere, namely the basal ganglia and thal amus, and the cortical regions to which they project and influence (Alexander et al., 1986) and b) hemispheric lateralization and specialization of f unction for emotional behavior (Liotti and Tucker, 1995). The current study addressed several issues pertinent to behavi oral sequelae of Parkinsons disease. First, this study examined lateralized subcortical contributions to expressivity. As subcortical structures have been shown to be influential in cognitive processing in asymmetrical 22

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PD presentation, it may affect emotional processi ng as well. Thus, we investigated whether the right cerebral hemisphere hypothesi s of emotional behavior is still supported when examining facial expressivity in PD. Second, the current study examined mood symptomatology via selfreport measures of depression and apathy in PD patients as a separate additional measure of emotional processing, which presents a more globa l perspective of patients emotional profile and may help discriminate emotional experience from expressivity. Finally, one of the unique aspects of the current study was the manner in which facial expressivity was measured and quantified. In contrast to most studies which involve subjective ratings of facial emotion by blinded judges (St. Clair et al., 1998; Blonder et al., 1989b), the present study used a computerbased imaging approach for quantif ying facial expressions. This approach involved videotaping participants while they posed different facial expressions in response to tone cues. Semiautomated computer software developed in Dr. Bo wers laboratory was then used to digitize each video frame of the dynamic expression. Th is method allowed us to capture both total movement of the face as well as the time it took to initiate the expression and the temporal trajectory of the entire expressi on. The time variables in this experiment were thought to be particularly important since slowness or brad ykinesia is one of the prominent features of Parkinsons disease. The current study had two specific aims. The primary aim was to learn whether onset side of Parkinsons disease motor symptoms was re lated to changes in pose d facial expressivity. To address this aim, PD patients with laterali zed symptom onset were evaluated in terms of quantitative aspects of their facial expression s. Based on the right hemisphere model of emotional behavior, it was hypothesized that PD patients with left-sided motor symptom onset, indicating greater right hemisphe re neuropathology, would display greater facial expressivity 23

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24 impairment than patients with right-sided motor symptom onset. Therefore, it was predicted that facial expressions posed by leftonset PD patients would entail overall less movement and would be slower to form than those posed by right-ons et PD patients, regardless of the particular emotion posed. The secondary aim of the present study was to exam ine the relationship between mood and disease-specific motor variables and PD pa tients facial expressi vity. Given previous research indicating the effect of nigrostriata l dopamine loss on emotional and motor functioning, it was hypothesized that depressi on and apathy as well as greate r motor disturbance would be associated with greater impairment in facial expressivity. Thus, it was predicted that higher scores on the self-report mood measures such as the Beck Depression Inventory (BDI) and the Apathy Evaluation Scale (AES) would correspond to slower and slighter facial movement. Similarly, it was predicted that increased severity of motor symptoms, particularly bradykinesia and rigidity, on the standard Unified Parkins on Disease Rating Scale (UPDRS) would also be associated with reduced facial expressivity.

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CHAPTER 3 METHODS Participants Participants included 26 patients with idiopathic Parkinsons disease and a healthy control group of 13 participants. Parkinsons disease pati ents were assigned to right or left symptom onset groups based on their self -report. Patients who descri bed bilateral onset of motor symptoms or could not recall their initial side of onset were not included. Patients were divided into groups based on onset side rather than current motor symp tom presentation because studies indicate that the classification of current si de predominance according to the UPDRS score oversimplifies the clinical pict ure and may be subjectively eval uated (Katzen et al., 2006; Tomer et al., 1993). The final PD sample included 13 patients with right-sided motor symptom onset (RSO-PD) and 13 patients with left-sided motor symptom onset (LSO-PD). Both PD patients and healthy control participants were recruite d through a larger NI NDS-funded study entitled Masked Faces in Parkinsons Disease: Mech anisms and Treatment being conducted in the Cognitive Neuroscience Laboratory at the University of Florida (Director: Dr. Dawn Bowers), and participated in the complete or partial pr otocol designed for the parent study. Additionally, several patients were recruited from the Univ ersity of Florida Movement Disorders Center, which maintains an extensive IRB and HIPAA-compliant database of current PD patients (Directors: Dr. Michael O kun, Dr. Hubert Fernandez, Dr. Kelley Foote). Patients included in the present study ha d to be between 45 and 80 years old and, according to the UK Brain Bank criteria for diagnosis of idiopathic Parkinsons disease, had to display the presence of bradykine sia and at least one other motor sign (rigidity, resting tremor, or gait disturbance) during their UPDRS Motor Ex amination (Hughes et al., 1992). Additionally, a positive response to dopaminergic therapy was requir ed to affirmatively diagnose idiopathic PD. 25

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Diagnosis of idiopathic PD was ruled out if patients had a history of traumatic brain injury, definite encephalitis, supranuclear gaze palsy, cerebe llar signs, or displayed signs of Parkinsons plus syndromes, such as Lewy body disease. Exclusion criteria for PD patients were as follows: (1) bilateral onset of Parkinsons disease (motor symptoms may be present on both sides of the body after in itial unilateral onset); (2) evidence of dementia or significant cognitive impairment; (3) evidence of a current or chronic major psychiatric or psychological disturba nce; (4) excessive oro-facial dyskinesias that interfere with their facial expr essivity; (5) unwillingness to shave facial hair or remove facial jewelry that would compromise the quality of the image capture, (6) history of deep brain stimulation or other surgical pr ocedures designed to treat PD motor symptoms; (7) evidence of Parkinsons plus syndromes (i.e., Lewy body di sease, corticobasal degeneration, multiple systems atrophy). Exclusionary cr iteria for healthy control partic ipants were the same as those for PD patients with the additional exclusion criterion of diagnosed unilateral or bilateral Parkinsons disease or parkinsonian symptoms. Healthy control participants were between the ages of 45-80 years old. As shown in Table 3-1, the two PD patie nt groups (RSO-PD and LSO-PD) and healthy controls were carefully selected from the pare nt study to be very well matched on demographic variables such as age, educa tion, sex, and handedness. Additionally, a review of patients medical records was performed in order to c onfirm unilateral onset side. A one-way ANOVA was conducted to ensure well-matched groups. Results of this ANOVA did not reveal statistical difference between the groups in age [F(2,38)= 0.41, p= 0.70] or education [F(2,38)= 0.52, p= 0.60]. The age range of the right-sided onset PD group (RSO-PD) was 52-76 years old (M= 67.69, SD= 7.10) and the age of left-sided onset PD patients (LSO-PD) ranged from 56-80 years 26

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old (M= 70.08 SD= 7.84). The age of healthy c ontrol participants ranged from 53-80 years old (M= 67.60, SD= 8.74). Each group had 8 males and 5 females, reflecting established sex-based differences in incidence of PD (Wooten et al., 2004). The RSOPD group and healthy controls each had 11 right-handed and 2 left-handed indi viduals while the LSO-PD had 10 right-handed and 3 left-handed participants. The groups, on aver age, were highly educated and did not present evidence of dementia as assessed by th e Mattis Dementia Rating Scale-II. The PD groups were also selected to be co mparable on duration of symptoms and total UPDRS motor score, as evidenced by insignificant differences in two-tailed independent samples t-tests conducted on these diseas e-specific variables [duration of PD symptoms, t(24)= 0.66, p= 0.52; total UPDRS score, t(24)= -0.52, p= 0.48]. The average duration of symptoms in the RSOPD group was 8.23 years (SD= 4.88 years) and the groups average UPDRS Motor score was 21.08 (SD= 8.25); the average duration of symptoms in the LSO-PD group was 7.08 years (SD= 4.01) with an average UPDRS Motor score of 24.15 (SD=10.00). Table 3-1. Participant Demographics RSO-PD LSO-PD Controls Significance Demographic N=13 N=13 N=13 Mean (SD) Mean (SD) Mean (SD) Age 67.69 (7.10) 70.08 (7.84) 67.62 (8.74) NS Education 16.46 (2.82) 16.23 (2.31) 15.46 (2.67) NS Sex Ratio (Male: Female) 8:5 8:5 8:5 NS Handedness (Right: Left) 11:2 10:3 11:2 NS DRS Score 140.77 (2.95) 137.62 (5.64) 139.85 (4.58) NS Duration of Symptoms (in years) 8.23 (4.88) 7.08 (4.01) NS UPDRS Total 21.08 (8.25) 24.15 (10.00) NS 27

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Measures Prior to enrollment, all PD patients underwent a thorough neurological examination to verify their diagnosis and rate th e severity of their motor symptoms All participants were also administered neurocognitive and psychiatric measures by a trained doctoral student to screen for dementia, cognitive impairment, significant psych opathology or other factor s that would exclude them from the study. These measures are listed below. Unified Parkinsons Disease Rating ScaleIII Motor Examination (UPDRS-III) (Lang & Fahn, 1987): The UPDRS-III is a tool used by neur ologists to assess the severity of various motor symptoms and impairment of daily living ac tivities in PD patients. Symptoms on the right and left side of the body are rated separately in areas of resting and actin g tremor, bradykinesia, and rigidity on a 0-4 scale with higher values i ndicating greater motor impairment. The range of possible scores on the UPDRS-III Motor Examination is 0 to 56. Mattis Dementia Rating S cale-II (DRS-II) (Mattis, 2001): The DRS-II is a screening measure for dementia in older adults with well -established psychometric properties that covers the domains of memory, atten tion, initiation, language, and vi suoconstruction. There are 144 possible points; a score of 125 or below s uggests significant evidence for dementia. Mental Health Screening Form-III (MHSF-III) (Carroll & McGinley, 2001): The MHSFIII is a brief structured psychiatric interview meas ure used to screen for mental health problems and refer identified cases for further diagnosis. Beck Depression Inventory-II (BDI) (Beck et al., 1996): The BDI-II is a self-report measure in which individuals are asked to rate the severity of symptoms associated with depression, such as sleep, appetite worthlessness, and anhedonia on a 0-3 Likert scale. There are 21 items on the BDI-II, yielding scores that range from 0-63 with higher scores indicating greater 28

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depressive symptoms and a score 14 suggesting mild to moderate depression. Levin et al. (1988) demonstrated that the BDI-II is a highly reliable and valid measure to assess depression, particularly in PD patients. Apathy Evaluation Scale-modified (AES) (Sta rkstein et al., 1992): Modified from the original 18-item AES created by Marin (1991), the modified AES is a 14-item scale assessing cognitive, emotional, and behavioral aspects of apathy on a 0-3 Likert scal e. Scores range from 0-42 with higher scores indicat ing higher apathy and a score 14 suggesting significant signs of apathy. The modified AES is shown to have exce llent psychometric properties in Parkinsons disease (Kirsch-Da rrow et al., 2006). Procedures All participants were asked to read and sign an informed consent agreement consistent with the University of Florida Institutional Revi ew Board and Federal HIPAA regulations at the commencement of the study. Following informed consent, all participants underwent the cognitive and psychiatric screening procedures and UPDRS-III motor scores were obtained for the PD patients. All PD patients were on medication during testing, meaning they were instructed to take their an ti-parkinsonian medication (i .e., Levodopa, dopamine agonists) according to their normal regimen on the day of testing. Videotaping of facial expressions. Subjects were videotaped with a black and white Pulnix camera (TM-TCN) and a Sony video reco rder (SLV R 1000). The camera was positioned approximately five feet in front of the patient. Indirect lighting was produced by reflecting two 150-watt tungsten light bulbs onto white photogr aphy umbrellas positioned approximately 3 feet from the face. Lighting on each side of th e face was balanced within one lux of brightness using a Polaris light meter. To reduce extraneous facial movement, subjects were reminded to 29

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not blink during the expression. To minimize head movement, an adjustab le head restraining device, the Vac-Loc Head Stabiliz ation system, was employed. The Vac-Loc system consists of a pliable plastic pillow filled with polystyrene beads. The pillow was molded around the subjects head, and then air was vacuumed from the bag to form a rigid mold to the individuals head, thereby effectively minimizing the impact of tremor or shifting. During testing, participants were asked to pose three emotional expressions, angry, fearful, and happy at the onset of a tonal cue. These three particular facial expressions were chosen for two reasons: a) they all have a strong, distinguishable affective quality, and b) they incorporate both positively and nega tively-valenced emotions. Each expression trial consisted of the experimenter informing the participant of the ta rget facial emotion. Part icipants were told to make the target emotion as soon as the tone cue was presented, and to make the expressions as distinctly and clearly as possible so that others would recognize the emotions they were trying to convey. Tone onset was controlled by the expe rimenter and was created by a hand-held buzzer synchronized to a light emitting diode (LED) pla ced within the video frame. The LED was subsequently used during the face digitizing proc ess to precisely measure the initiation of the expression from the onset of the tonal cue. Pa rticipants were asked to produce each expression twice to increase the chances of obtaining a tr ial free of extraneous motion or artifact. Data processing of videotaped facial expressions. First, videotaped facial expressions were viewed by two trained raters who independently viewed each expression and selected those with the least motion artifact. Next, individual expressions were digitized using a Sony video player, personal computer with Iscan-PCI video card, and EYEVIEW software (Imaging Technology). Beginning with the onset of the trial (e.g., after the tone cue sounds), 90 video frames (3 seconds or 30 frames/second) were captured for each expression and saved on the 30

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computer to be analyzed. Finall y, the digitized video facial expr ession images were quantified in terms of movement changes using custom comput er software, previously developed by Didem Gokcay in the Cognitive Neuroscience Laboratory at the University of Florida. This software, known as Computer Human Expression Evaluation System (CHEES), enables semi-automatic processing and quantification of faci al expression data (Bowers et al ., 2006). In order to process the expression, sixteen anatomic landmarks were first identified on the target face and denoted on the first frame of an expression sequence. CH EES then uses these landmarks to automatically compute nine geographic boundaries or regions of interest (ROIs) that are applied to all subsequent frames of a particular expression (See Figure 3-1). These ROIs are compared over consecutive frames to establish movement cha nges via an entropy calculation. Entropy is defined as a measure of pixel intensity changes that occur duri ng a dynamic expression. It is calculated by subtracting the values of corresponding pixe l intensities between adjacent frames, summing their differences, and dividing that amount by the number of pixels used. This computation is repeated over each pair of successive frames, yielding 89 difference images over 90 frames. Entropy is a valid and reliable fa cial expression qualifier that i ndicates a normalized value with respect to individual differences in faces (Bowers et al., 2006). In the present study, only the lower 2/3 of th e face (from beneath the eye to the bottom of the chin) was analyzed. The decision to restrict analyses to the lower 2/3 of the face was based on theoretical reasons and practical concerns. Theoretically, move ment in the lower 2/3 of the face is controlled primarily by contralateral hemispheric projections while the upper face is controlled bilaterally. Thus, expressivity in th e lower 2/3 of the face is more influenced by asymmetrical neuropathophysiology, which is of primary interest in the current study. 31

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Practically speaking, focusing on the lower 2/3 of the face also eliminated extraneous movement caused by occasional eyeblinks in some participants. Figure 3-1. Digitizing the Moving Face. The face is first landmarked using 20 anatomical points. Then, these marks are used to partition th e face into 9 regions of interest based on muscular boundaries, which will be used to derive entropy and temporal variables of dynamic movement. Dependent variables. Five major outcome variable s were derived from the CHEES process: 2 entropy variables and 3 temporal variables. The tw o entropy variables included total entropy (total amount of movement change duri ng a dynamic expression), and peak entropy (the most rapid movement change that occurs when the expression can first be identified for its emotion). The three temporal variables, measured in seconds, included latency, or initiation time between the tonal cue and facial movement, rise time to peak entropy, and duration of movement. The entropy curve and temporal point s along the curve are depi cted in Figure 3-2. Statistical Analyses To evaluate the Aim 1 prediction that LS O-PD patients would display greater overall facial expressivity impairment than RSO-PD patients and controls, 5 separate Repeated Measures ANOVAs were conducted, one for eac h of the 5 dependent variables described previously. For each ANOVA, the within-subjects factor was Emo tion expressed (angry, fearful, and happy) and the between-subjects factor was Group (RSO-PD, LSO-PD, and controls). 32

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33 To test the Aim 2 prediction th at greater mood and motor dist urbance would be associated with decreased facial expressiv ity, a series of linear regressi on analyses were conducted on each of the 5 facial expression depende nt variables. First, in or der to evaluate the association between mood (i.e., depression and apathy) and expressivity, scores on the Beck Depression Inventory (BDI-II) and Apathy Evaluation Scalem odified (AES) were examined in relation to the facial expressivity variables. A second set of linear regressions l ooked at the relationship between motor disturbance in PD patients and facial expressivity. The motor disturbance variables included composite scores derived from the Unified Parkinson Disease Rating Scale (UPDRS), specifically the bradykinesia/ rigidity score and a tremor score. R1 <<<<< <<<<<<<< <<<<<<<<<<< <<<<<<<<<<<< <<<<<<<<<<<<<< <<<<<<<<<<<<<< <<<<<<<<<<<<<<< <<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<<<<<<<<<<<< E1 E2 P ea k E n t ropy BaselineR2 Total Entropy (E1 + E2) End of movement Expression appears most intense Beginning MovementP Time Cue R1 <<<<< <<<<<<<< <<<<<<<<<<< <<<<<<<<<<<< <<<<<<<<<<<<<< <<<<<<<<<<<<<< <<<<<<<<<<<<<<< <<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<<<<<<<<<<<< <<<<< <<<<<<<< <<<<<<<<<<< <<<<<<<<<<<< <<<<<<<<<<<<<< <<<<<<<<<<<<<< <<<<<<<<<<<<<<< <<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<<<<<<< <<<<<<<<<<<<<<<<<<<<<<<<<<<< E1 E2 P ea k E n t ropy BaselineR2 Total Entropy (E1 + E2) End of movement Expression appears most intense Beginning MovementP Time Cue Figure 3-2. Entropy Curve. The outcome variab les in the current study are as follows: (1) Total Entropy (E1 + E2) = total amount of movement cha nge during a dynamic expression; (2) Peak Entropy (E1) = most rapid movement change (corresponding to the point of initial emotion categorization by observers; (3) Latency (time between R1 and cue) = initiation time to expression; (4) Rise Time ( P R1) = time to peak movement change; (5) Duration (R2-R1) = total time of dynamic movement change.

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CHAPTER 4 RESULTS The Effect of Laterality on Facial Expressivity The primary focus of this study was to examine differences in facial expressivity between Parkinsons disease patients with right-sided motor symptom onset (RSO-PD) and those with left-sided onset (LSO-PD) as well as healthy controls with the prediction that LSO-PD would be more impaired in performing facial expressions than the other groups. To accomplish this, the groups were compared on 5 aspects of facial expr essivity: (1) total entr opy, (2) peak entropy, (3) latency to expression, (4) rise time to peak entropy, and (5) duration of movement. Five independent Repeated Measures ANOVAs were conducted with Group (RSO-PD, LSO-PD, and controls) as the between -subjects variable and Expression (H appy, Angry, Fearful) as the withinsubjects variable. SPSS computer software was us ed to complete all analyses. The assumption of sphericity was successfully met in all 5 analys es; therefore, no corrections were necessary in omnibus reports. Regarding entropy variables, ANOVA results indicate no significant main effects of Group in either total entropy, F(2,36)= 0.28, p= 0.75, p 2 = 0.02, or peak entropy, F(2,36)= 0.36, p= 0.70, p 2 = 0.02. In other words, the three groups did not significantly differ in the total amount of dynamic movement during the facial expression or in the peak movement change. Entropy means and standard deviations for the three groups are shown in the Appendix, Table A1. However, there was a significant main eff ect of Emotion for total entropy [F(2,72)= 11.24, p< 0.05, p 2 = 0.24]. Bonferroni-corrected post hoc comparisons indicated that posing Happy expressions (M= 1.58, SD= 1.21) involved significantly greater total entropy (i.e., movement) than posing Angry (M= 0.82, SD= 0.83) or Fearfu l expressions (M= 0.85, SD= 0.92) at alpha = 0.05. Similarly, there was also a main effect of Expression when examining peak entropy, 34

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F(2,72)= 7.38, p< 0.05, p 2 = 0.17. Bonferroni-corrected post hoc comparisons revealed that, again, the Happy expression (M= 11.86, SD= 7.35) had a higher peak entropy, or rate of change, than the other two expressions at alpha = 0.05 (Angry: M= 6.42, SD= 6.93; Fearful: M= 7.99, SD= 8.63). The Group x Expression interaction was not significant for ei ther total entropy or peak entropy; thus, the groups did not differ in total amount of movement [F(4,72)= 1.13, p= 0.35, p 2 = 0.06] or peak rate of change [F(4,72)= 1.34, p= 0.26, p 2 = 0.07], regardless of emotion posed. A summary of the results from these ANOVAs is shown in the Appendix, Table A-2. In analyzing the three temporal variables, the only significant main effect of Group was latency to expression, F(2,36)= 8.21, p= 0.001, p 2 = 0.31. Bonferroni-corrected post hoc analyses revealed that the LS O-PD group (M= 3.62 s, SD= 2.86 s) was significantly slower in initiating movement following the tonal cue than the RSO-PD (M= 1.85 s, SD= 1.45 s) or Control groups (M= 1.59 s, SD= 1.63 s) at alpha = 0.05. Thus, the LSO-PD group initiated their expressions approximately 2 seconds later on aver age than the other two groups. There was also a significant main effect of Expression [F(2,72)= 3.56, p= 0.03, p 2 = 0.09]; post-hoc analyses (Bonferroni-corrected) reveal ed that the Angry expressi on (M= 3.04 s, SD= 2.72 s) was significantly slower to initiate than the Fearfu l expression (M= 2.04 s, SD= 2.26 s, p< 0.05) or the Happy expression (M= 1.98 s, SD= 1.79 s, p< 0.05). The Group x Expression interaction was nonsignificant [ F(4,72) = 0.82, p= 0.52, p 2 = 0.04.] In examining the rise time to peak expression, none of the main effects nor the in teraction reached significance [Group: F(2,36)= 1.32, p= 0.28, p 2 = 0.07; Expression: F(2,72)= 0.18, p= 0.84, p 2 = 0.01; Group x Expression: F(4,72)= 0.61, p= 0.66, p 2 = 0.03]. Similarly, an analysis of expression duration revealed no significant main effects or intera ctions [Group: F(2,36)= 0.35, p= 0.71, p 2 = 0.02; Expression: 35

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F(2,72)= 2.31, p= 0.11, p 2 = 0.06; Group x Expression: F(4,72)= 1.11, p= 0.36, p 2 = 0.06]. In other words, the three groups were comparable in terms of rise time and duration of expression, regardless of affect posed. Descriptive sta tistics as well as ANOVA results for temporal variables measured are presented in the Appendix, Tables A-3 and A-4, respectively. To sum the results from the primary aim, onl y one dependent variable, time to initiate a facial expression, proved to be a significant difference among the groups in the direction predicted. Namely, PD patients with left symptom onset were slower to initiate facial expressions than the other two groups (See Figure 4-1). The groups did not differ in entropy or other temporal variables. Fam ily-wise, 1 of the 5 outcome variables, or 20% of the analyses conducted, reached significance, demonstrating a small to moderate effect as opposed to a chance finding. These results are somewhat surpri sing given past research showing a significant difference in total amount of faci al entropy between PD patients a nd healthy controls (Bowers et al., 2006); possible reasons for this discrepanc y will be discussed in the following section. 0 1 2 3 4 5 6 7 RSO-PD LSO-PD Control GroupLatency to Expression (in seconds) RSO-PD LSO-PD Control Figure 4-1. Latency to Initiate Facial Expression in rightsided motor symptom onset PD patients, left-sided motor symptom onset PD patients, and healthy controls. Latency refers to time, in seconds, between tone cue and expression onset. 36

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Mood and Motor Correlates of Expressivity A secondary aim of this study was to exam ine the relationship among mood variables (depression, apathy), PD-specific disease variables (motor sympto ms) and facial expressivity. Initial one-way ANOVAs and inde pendent samples t-tests were conducted to learn whether the participant groups differed in terms of depression (BDI), apathy (AES), or severity of motor symptoms. Motor symptoms included composite scores for bradykinesia/ rigidity and tremor from the Unified Parkinson Disease Rating Scal e (UPDRS). Table 4-1 depicts the means and standard deviations of mood and motor symptom sc ores for the 3 subject groups. Results of the ANOVAs revealed no significant group differences for the BDI [F(2,36)= 0.50, p= 0.61] or the AES [F(2,36)= 0.91, p= 0.41]. Similarly, the t-tests indicated that ther e were no significant differences between the two PD groups in sever ity of bradykinesia/rigi dity [t(24)= -0.72, p= 0.48] or tremor scores [t(24) =0.91, p= 0.24]. Table 4-1. Descriptive Statistic s for Mood and Motor Variables RSO-PD LSO-PD Controls Significance Variable N=13 N=13 N=13 Mean (SD) Mean (SD) Mean (SD) Mood BDI 5.46 (3.60) 4.85 (4.16) 3.85 (4.69) NS AES 9.00 (5.03) 10.54 (6.06) 7.92 (3.50) NS Motor Tremor 1.69 (1.49) 2.38 (1.45) NS Bradykinesia/ Rigidity 12.23 (5.00) 13.92 (6.85) NS Relationship between Mood and Facial Expressivity Linear regression analyses were conducted to examine the effect of mood (BDI-II, AES) on the five facial expression variables (total entropy, peak entropy, late ncy, rise time, total duration). All participants we re grouped together and the outcome variables were averaged across the expression type posed. It was predicted that higher scores on the Beck Depression 37

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Inventory (BDI-II) and Apathy Evaluation Scalemodified (AES) would be associated with reduced facial movement (total entropy, peak entropy) and longer/slower movement times (i.e., initiation time, rise time, duration). The results of the linear regression an alyses are depicted in Table 4-2. As shown, the mood variables of depression and apathy did no t significantly explain variance in any of the 5 facial expressivity vari ables. There was a trend towards significance in the effect of the BDI-II on duration of expression [ = -0.59, t(2,38)= -1.92, p= 0.06]; however, the overall model did not reach significance, R2 = 0.10, F(2,38)= 2.03, p= 0.15. Because motor symptom onset side significantly affected the latency variable in facial expressivity, a hierarchical regression was conducted with onset side in Block 1 and the mood variables in Block 2 to see whet her depression and apathy contribute d to this facial expressivity variable. Results indicate that the overall model was significant [R2 = 0.32, F(4,34)= 4.01, p= 0.01], but that only left-sided onset uni quely contributed to the relationship ( = 0.53, t(4,34)= 0.53, p< 0.01). Neither mood score effectively explained variance in the model [BDI-II: = 0.09, t(4,34)= 0.61, p= 0.55; AES: = -0.03, t(4,34)= -0.17, p= 0.86]. Th us, change statistics did not reveal an additional effect of mood on the relationship between onset side and latency as evidenced by the negligible change in R from 0.31 to 0.32 in the hier archical regression [F change test: R2 = 0.01, F(2,34)= 0.18, p= 0.83]. However, this analysis confirmed the impact of left-sided motor symptom onset on latency, as this independent variable accounted for 31% of the variance. These results s hould be interpreted with caution however, as the relatively low number of participants per regressor in this analysis may severely limit power. 38

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Table 4-2: Linear Regression Analysis of Mood Variables on Facial Expressivity M (SD) R2 p-value Total Entropy (N=39) 1.09 (0.75) 0.003 BDI-II -0.05 0.78 AES 0.05 0.79 Peak Entropy (N=39) 8.76 (5.57) 0.03 BDI-II -0.16 0.36 AES 0.16 0.37 Latency (N=39) 2.36 (1.63) 0.02 BDI-II 0.07 0.70 AES 0.10 0.58 Rise Time (N=39) 2.43 (1.54) 0.02 BDI-II -0.02 0.91 AES 0.13 0.48 Duration (N=39) 2.54 (2.48) 0.10 BDI-II -0.59 0.06T AES 0.03 0.91 T= Trend towards significance. The Relationship between Motor Symptoms and Expressivity To assess whether PD motor symptoms had an effect on facial expressivity, motor symptoms of bradykinesia/rigidity and tremor were regressed on the 5 facial expressivity variables. All PD patients were combined into a common group of 26 participants; healthy controls were not included in this analysis. Collinearity diag nostics did not reveal significant multicollinearity issues with these two regressors. The results of the linear regression analyses are depicted in Table 4-3. As shown, neither bradykinesia/rigi dity nor tremor scores were positively associated with any of the facial expressivity variables at alpha = .05. An additional hierarchical regression anal ysis was conducted speci fically on the latency variable as it was significantly affected by left-onset group status in the primary aim. The PD patient groups (RSO-PD and LSO-PD) were in cluded in Block 1 and UPDRS motor symptoms (bradykinesia/rigidity and tremor) were placed in Block 2 to see whether patients motor symptomatology explained additional variance in facial expressivit y. Results demonstrated that while the overall model was significant [R2 = 0.35, F(3,22)= 3.95, p= 0.02], the motor symptoms 39

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40 did not uniquely contribute to the relationship [bradykinesia/rigidity: = 0.08, t(3,22)= 0.42, p= 0.68; tremor: = 0.19, t(3,22)= 0.97, p= 0.34]. Left-sided onset remained the only significant regressor [ = 0.49, t(3,22)= 2.77, p= 0.01]. The F-change test confirmed the negligible contribution of motor symptomatology to the relati onship between left-onset side and latency to expression, revealing an R2 change from 0.30 to 0.35 with the added regressors in Block 2 [Fchange test: R2 = 0.05, F(2,22) = 0.84, p= 0.44]. As was th e case with regressing both mood and onset side in the previously mentioned analysis these results must be interpreted with caution, for the low number of subjects per regressor may affect power. Table 4-3: Linear Regression Analysis of Motor Variables on Facial Expressivity M (SD) R2 p-value Total Entropy (N=26) 1.04 (0.79) 0.002 Bradykinesia & Rigidity -0.03 0.91 Tremor 0.04 0.85 Peak Entropy (N=26) 9.06 (6.10) 0.01 Bradykinesia & Rigidity -0.09 0.70 Tremor 0.10 0.67 Latency (N=26) 2.74 (1.65) 0.12 Bradykinesia & Rigidity 0.11 0.62 Tremor 0.29 0.19 Rise Time (N=26) 2.36 (2.20) 0.10 Bradykinesia & Rigidity -0.23 0.30 Tremor 0.13 0.55 Duration (N=26) 6.85 (4.37) 0.02 Bradykinesia & Rigidity 0.12 0.61 Tremor -0.13 0.56

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CHAPTER 5 DISCUSSION The primary aim of the present study was to i nvestigate the effect of asymmetric motor symptom onset in Parkinsons disease (PD) on emotional behavior as defined by facial expressivity. The masked face of PD can shar ply impact effective communication with family and caregivers, yet is relatively understudied among the cardinal motor symptoms in PD. Even more rarely examined is the effect of motor symptom onset laterality on emotional expression. Thus, this project was undertaken to examine the relationship between hemispheric laterality and different aspects of facial expres sivity. It was predicted that PD patients with left-sided motor symptom onset would have reduced facial expressivity, both in degree and timing, than patients with right-sided motor symptom onset. This prediction was based upon the well-supported right hemisphere hypothesis of emotion, which states that the right cerebra l hemisphere is dominant in the perception and expression of emotional behavior. Drawing fr om this model, it was posited that right subcortical dysfunction, as is seen in PD patients with left body side motor symptoms, would result in similar emotional deficits. A se condary aim was to discover the impact of mood and motor symptoms on facial expressivity with the prediction that worse symptoms would be positively correlated with expressivity impairment. This idea was based upon research suggesting that diminished facial expressivity in PD may be re lated to both emotional and motor disturbances (Simons et al., 2004) The overall purpose of this study was to examine the effect of asymmetric neuropathology upon the masked face in Parkinsons disease. Summary and Interpretation of the Findings The hypothesis that left-sided motor symptom onset PD patients (LSO-PD) would be less facially expressive than those with right-sided onset (RSO-PD) was not entirely supported. The groups differed only in latency to initiate target facial expressi ons. Namely, PD patients whose 41

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motor symptoms initially presented on the left body side (i.e., right brain involvement) were significantly slower to initiate their expressions, regardless of valence, than PD patients with right body symptoms and healthy control participants. The other as pects of facial expressivity, including entropy, rise time to peak movement, and movement duration, were not influenced by laterality of symptom onset. Neither mood symptoms, such as depression and apathy, nor motor symptom variables of bradykinesi a, rigidity, and tremor contri buted to changes in facial movement. These findings do not robustly support th e right hemisphere hypothesis of emotion, upon which the predictions from this study were ba sed. Only one measure, initiation time, was influenced by laterality of PD symptoms. T hus, greater damage to the basal ganglia-thalamocortical loops in the right hemis phere, as is the norm in PD patie nts who present with left-sided symptoms, did not negatively impact facial emot ional behavior as defi ned by overall movement and duration during posed facial expressions. The data also do not support the bivalent hemisphere emotion mode (i.e., nonsignificant Group X Emotion interaction). According to this model, negative emotions such as fear and ange r are mediated more so by the right hemisphere, and positive emotions, such as happiness, by the left hemisphere. Therefore, it seems that neither model of hemispheric late ralization of emotion appropriatel y accounted for the results of the present study. There are several possible factors that may contri bute to the failure to support either model. One possibility relates to the nature of the facial expressions that were posed by the participants. For instance, it may be argued that, because partic ipants were asked to look happy, frightened, or angry, they were not expressing true emotion. Thus, the expressions occu rred in response to a command rather than arising from particular affective states. A lthough a variety of studies have 42

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found that posing an emotion on the face can actually induce psychophysiological changes associated with true emotions (Lee et al ., 2006; Ekman, 1992; Adelmann & Zajonc, 1989), we have no independent verification that participants in the pres ent study experienced emotions associated with the expressions they were aske d to produce. Moreover, a large neuroanatomic literature has drawn a distincti on between voluntary (posed) and s pontaneous facial expressions, with each being mediated by somewhat distinct neural circuitries (R inn, 1984). The former (posed) is primarily mediated by frontal pyramidal systems of the brain, whereas the latter (spontaneous) involves more limbic and extrapyramid al regions. Following from this argument, emotional processing centers in the brain may not have been involved in the present study. One way to better address this would be to examin e whether side of PD symptom onset influences spontaneous facial expressivity. Another possible reason why th e results did not support eith er model of hemispheric lateralization of emotion is that motor symptom onset is not necessarily indicative of the current state of neurodegenerati on. While motor symptoms usually remain worse on the body side of initial presentation, this is not always the case. In the current sample, motor scores from the Unified Parkinson Disease Rating Scale (UPDRS) recorded directly prior to study participation revealed a discrepancy between laterality of sy mptom onset and current symptom laterality in 6 of the 26 PD patients. Two PD patients had sl ightly higher values (e.g., greater pathology) on the body side opposite of their onset presentation, whereas 4 patients had equally bilateral motor symptoms at the time of testing. Although thes e scores do not indicate that those specific patients have switched motor symptom side as the difference between right and left motor symptoms in these cases were very slight, it do es show that motor asymmetry in PD is not always a stable characteristic. Additionally, bilateral dysfunction may be present when motor 43

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symptoms are first apparent despite unilatera l presentation. Neurophysio logical studies have confirmed that even in hemi-parkinsonism, there is almost always some degree of bilateral subcortical damage, which must be taken into ac count when assessing func tional lateralization in PD (St. Clair et al., 1998). Thus, perhaps the current study could not accurately portray activation of parallel emotional pathways in the two hemispheres as the damage to the basal ganglia circuits may have already been bilateral. Despite this caveat, most studies suggest that even with bilateral dysf unction, there is some asymmetry, as ev idenced by the plethora of studies examining structural and functional correlates of lateralized motor symptoms in PD. Latency to Expression as an Action-Intentional Deficit The primary finding of the present study was that the left-onset PD patients were slower in initiating facial expressions than the other two comparison groups. This slower response by the left-onset group was present across all expressi ons and appeared to represent a more global defect in rapidly initiating movement in the f ace. Bowers et al. (2006) also reported facial bradykinesia in a small group of more severe ly affected PD patients who posed facial expressions. However, these authors did not di sentangle initiation time from overall movement time and were therefore unable to determine wh ich of these two pro cesses, initiation or execution, accounted for the slowing. The findings of the present study, however, seem to imply that it is the time to initiate facial movement that is slowed in left-onset PD patients, and that, once commenced, the expression occurs within a normal temporal window. Turning to the literature, there are few st udies that have asso ciated slowed motor processing with laterality of symptom onset. Some investig ators (Zetusken & Jankovic, 1985) have posited that PD patients w ith greater left-sided disease are more likely to exhibit overall slowness and rigidity th an patients who initially present with right-sided symptoms. These observations have not been described in other reports, and currently there is very little 44

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information as to whether greater left-sided sy mptoms are associated with a slowed response time to external stimuli. One key question concerns the basis for the sl owed initiation of facial movements by the left symptom onset PD patients in the present study. What might account for this laterality effect in initiation time? In revi ewing the neuropsychology and beha vioral neurology literature, a variety of studies over the past 30 years have reported that focal lesions of the right hemisphere induce slowed reaction times on va rious cognitive and motor tasks, whereas this effect is not seen in patients with left hemisphere lesions (Coslett and Heilman, 1989; De Renzi & Faglioni, 1965; Heilman and Boller, 1975). These findings, c oupled with a vast literature on hemispatial neglect following right hemisphere lesions (M eador et al., 1989; Ga inotti et al., 1972) and various attentional studies in t hose without brain damage (Petit et al., 2007; Stevens et al., 2005) have led some to posit that the right hemisphere plays a special role in mediating intention, or the physiological readiness to respond (Heilman, Wa tson, & Valenstein, 2003). This has been identified as the right hemisphere attention/intention hypothesis. Extending this line of reasoning to the presen t study, perhaps the slowed facial expression initiation time by the left-symptom onset PD pati ents reflects a dominant role of the right hemisphere in mediating readiness to respond. In other words, the significant finding may actually stem from an action-intention deficit, associated with righ t hemisphere dysfunction, rather than defective emotional processing, as orig inally predicted. In order to fully test the hypothesis that left-sided onset PD patients are slower to initia te their expre ssions due to a greater deficit in intentional behavior, it would be necessary to more broadly examine the performance of PD patients across a series of timed tasks with si gnal/warning cues. Thus, more 45

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studies must be conducted prior to further specu lation on this post-hoc ex planation of the finding in the present study. The second aim of the present study examined mood and motor corr elates of facial expressivity, with the prediction that greater severity of depre ssion and apathy as well as more severe symptoms such as bradykinesia and rigidity would negatively impact facial movement during emotional expressions. However, regression analyses did not reveal a significant contribution of mood or specific motor symptoms to changes in facial expressivity; moreover, they did not affect the relati onship between left-sided onset and latency to expression in additional analyses. Several factors could accoun t for the insignificant findings. As mentioned earlier, the posed facial expre ssions may not have elicited the experience of emotion, and, therefore, emotional centers in the brain may not have been activ ated. If this is the case, the participants mood would have very little to do with th eir ability to pose th e particular facial expressions. Thus, an examination of the e ffect of mood on spontane ous facial expression derived through known emotional experience may be more revealing. Another factor is that the range of mood and motor symptom scores may not have been sufficiently large enough to allow for adequate correlation with faci al expression variables. As a group, the participants were not depressed or apathetic and the severity of PD symptoms was moderate. Finally, the facial variables themselves represented quantitative indi ces of facial movement, rather than subjective ratings of emotion by independent judges. It is possible that subjective ratings, which involve more of a gestalt impression, might relate more so to mood and ratings of motor severity. Limitation of the Present Study The current study had several limitations. First, the number of participants in each group was less than originally desired, and may ha ve considerably limited the power of the relationships tested, thereby potentially preclud ing significant findings in several analyses. 46

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However, given the weak effects of group on faci al expressivity observed in 4 out of the 5 outcome variables in the primary aim and the minimal unique contributions of mood and motor variables reported in the secondary aim, it is doubt ful that a true relati onship exists in these analyses using the current sample. Additionally, the lack of ethnic and r acial diversity in the current sample may have significantly reduced th e external validity of the results. Amongst 39 participants, there were only 2 African-Americans tested (1 RSOPD and 1 healthy control) and the rest were identified as Non-Hispanic Caucas ian. Although there is curr ently no firm data to suggest racial or ethnic differences in the prev alence, presentation, or course of Parkinsons disease, the results of this st udy are nonetheless limited in terms of generalizability to a broader population. Another limitation of the current study is that there may have been a selection bias in our sample as participants were recruited from a la rger study also examining facial expressivity in PD, but not specifically the influenc e of laterality. Because of this crucial feature in the current study, several participants were excluded from analyses for vari ous reasons (i.e., bilateral or unknown onset) while others were selected to cr eate equal, matched groups. Furthermore, because evidence of a major psychiatric disturba nce was an exclusion criterion in the larger study, participants with depression as measured by the BDI were also ex cluded in the present study. Depression in the PD groups may have been especially interesting to examine given the emotional focus of the study and the hypotheses c oncerning hemispheric roles in emotion. Thus, there may be a chance that the current sample a nd subsequent results may not have accurately represented the greater p opulation given the goals of the present study. There were also concerns regarding the methodology of our study. The decision to use posed expressions rather than those induced by ac tual emotion may have limited the activation in 47

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the extrapyramidal pathways described earlier. In other words, by potentially reducing the involvement of emotional centers in the brain, the differences in true emotional expression between groups may not have been captured. Of note, Bowers et al. (2006) had found that PD patients exhibited less entropy than healthy controls in posed expressions, thereby providing support for the idea that both cortical and subcorti cal enervations of the f ace are affected by PD. However, because the goal of the present study was to examine the eff ect of laterality on emotional behavior rather than to understand the nature of dimi nished facial expressivity, an analysis of spontaneous expressivity may still have been more indicative of asymmetrical emotional dysfunction. Another methodological con cern in the present study was the decision to only examine PD patients when fully on their levodopa therapy. This decision was made because we wished to reveal any noticeable differences in expressivity between the PD patients and controls in their normal, daily state of functioning. While this look at facial expressivity in PD is highly ecologically valid, it may have negated some differences between groups by placing the patients levels of motor functioning cl oser to that of healthy controls. Another notable limitation in the current study wa s its failure to replic ate the results in the Bowers et al. 2006 study, which used the same face digitizing procedure in a group of 12 PD patients and 12 controls and found that patients exhibited signif icantly less entropy during their expressions than the control gr oup. Following this finding, it was expected that the two patient groups in the current study, regardless of how th ey compared with each other, would at least display reduced facial expre ssivity compared to the cont rol group. There are several methodological differences that may account for this disparity. First, the sample of patients in this study presented with mild to moderate PD, and some only had unilateral symptoms, qualifying them as Stage 1 in the disease acco rding to the Hoehn and Yahr Rating Scale. 48

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Because diminished facial expressivity is more no ticeable in later stages of PD, the current study may not have captured the differences in facial expressivity as the Bowe rs et al. (2006) study was able to do through inclusion of more severely affected patients. Secondly, the present study only examined the lower 2/3 of the face while Bo wers et al.s results were based on the whole face. Excluding emotional expressivity ar ound the eyes most likely significantly reduced entropy values. Thus, by controlling for extraneous movement, the results of the current may not be telling the whole story regard ing differences between groups in facial movement during an emotional expression. Directions for Future Research To address some of the limitations of th e present study, several changes in methodology may be made in future paradigms. First, spont aneous expressions, which are also collected from participants in the Cognitive Neur oscience Laboratory, may be used instead of posed expressions to assess this aspect of emotional behavi or. To induce involuntary emotional expression, participants are shown clips from humorous or disgusting television shows (i.e., Americas Funniest Home Videos, Fear Factor, etc.) and isolated expressions are selected to be digitized. While spontaneous expressions are more difficu lt to capture as there is often uncontrollable extraneous movement such as blinking or head shaking during laughs, they would afford a better look at emotional experience and subsequent expr ession in the three groups. Another change that could be made for future studies would be to compare the emotional expressions of right and left motor symptom onset PD patients when not on their levodopa medication. This analysis is perfectly feasible in the near future as PD patients are tested both on a nd off their medication in our laboratory using the same protocol. Given the results of the current study, it is predicted that there would be an even greater difference between right-sided and le ft-sided onset PD patients in 49

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their expression initiation time and perhaps in othe r temporal variables that require intentional movement, such as rise time to peak expressivity. Conclusion While the results of the pres ent study did not su pport the right hemisphere hypothesis of emotional behavior as originally predicted, they may be interpreted in terms of hemispheric differences in controlling intentional behavior. The highly significant finding that patients with left-sided motor symptom onset displayed greater latency to expression is thought to reflect greater dysfunction in the right he misphere via nigrostriatal dopami ne depletion characteristic of Parkinsons disease. As the experimental design requires part icipants to respond to a sounded cue with a posed facial expression, it can be viewed as a reaction time task in which one must perform an intentional act. Becau se intentional deficits are more commonly associated with right hemisphere damage, it is believed that the patients who presented with left-sided motor symptoms in our study demonstrated defective ac tivational behavior as opposed to dysfunctional emotional processing. The findings from this study are both clinically and scientifically rele vant. The ability to communicate through facial expressi ons is often taken for granted as it is an automatic process for most individuals. Timing is an essential part of facial expressi vity for it lets others know that you are present and engaged. If the timing of a facial expression is delayed, even by a few seconds as seen in the left-onset patients in this study, it can be very disconcerting to those on the receiving end. It has been mentioned previous ly that depression may be overdiagnosed in PD patients as clinicians may misattribute diminished facial expressivity and prosody for disturbed mood. A dissonant reaction during a conversatio n may lead health care workers to assume emotional problems in patients as well. To conclude, the current study may generate more research on action-intention di sorders in PD and how they differ from the cardinal motor 50

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51 symptoms of the disease. Also, our study may stim ulate interest in the e ffect of asymmetrical symptomatology in Parkinsons disease in domains other than cognition.

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APPENDIX DESCRIPTIVE STATISTICS AND ANOVA TABLES FOR PRIMARY AIM Table A-1. Descriptive Statis tics for Entropy Variables Outcome Variable (Entropy) RSO-PD LSO-PD Control M (SD) M (SD) M (SD) Total Entropy Group 0.96 (1.07) 1.13 (0.92) 1.17 (0.90) Expression Angry 0.95 (0.95) 0.86 (0.94) 0.66 (0.58) Fearful 0.54 (0.64) 0.80 (0.86) 1.22 (1.12) Happy 1.39 (1.61) 1.73 (0.96) 1.63 (1.01) Peak Entropy Group 6.13 (7.45) 9.84 (8.32) 8.14 (6.89) Expression Angry 8.21 (8.49) 7.28 (6.93) 3.78 (4.47) Fearful 6.46 (6.37) 8.82 (10.73) 8.69 (8.73) Happy 10.17 (7.49) 13.43 (7.31) 11.97 (7.48) Table A-2. ANOVA Summary : Entropy Variables Outcome Variable (Entropy) SS MS F p p 2 Observed Power Total Entropy Group 0.99 0.49 0.28 0.75 0.02 0.09 Error (Group) 62.63 1.74 Expression 14.45 7.22 11.24 <0.001* 0.24 0.99 Error (Expression) 46.29 0.64 Group x Expression 3.44 0.86 1.34 0.26 0.07 0.40 Peak Entropy Group 69.55 34.77 0.36 0.70 0.02 0.10 Error (Group) 3472.54 96.46 Expression 610.19 305.10 7.38 .001* 0.17 0.93 Error (Expression) 2978.50 41.37 Group x Expression 187.65 46.91 1.34 0.26 0.07 0.34 *= significant finding at alpha level 0.05. 52

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53 Table A-3. Descriptive Statisti cs for Temporal Variables Outcome Variable (Temporal) RSO-PD LSO-PD Control M (SD) M (SD) M (SD) Latency Group 1.85 (1.45) 3.62 (2.86) 1.59 (1.63) Expression Angry 2.51 (1.72) 4.79 (3.42) 1.82 (1.89) Fearful 1.85 (1.70) 2.79 (3.26) 1.49 (1.29) Happy 1.21 (0.93) 3.28 (1.89) 1.46 (1.70) Rise Time Group 1.74 (1.42) 3.25 (4.01) 2.91 (4.52) Expression Angry 2.31 (1.82) 2.49 (2.41) 3.59 (5.99) Fearful 1.33 (1.15) 3.85 (5.78) 3.03 (5.33) Happy 1.56 (1.28) 3.41 (3.83) 2.10 (2.25) Duration Group 6.83 (6.62) 6.88 (4.93) 8.19 (6.92) Expression Angry 7.23 (5.65) 7.21 (5.34) 11.31 (8.87) Fearful 6.46 (8.24) 7.69 (5.82) 7.95 (8.58) Happy 6.79 (5.99) 5.74 (3.65) 5.31 (3.29) Table A-4. ANOVA Summary: Temporal Variables Outcome Variable (Temporal) SS MS F p p 2 Observed Power Latency Group 858.58 429.29 8.21 0.001* 0.31 0.95 Error (Group) 1882.87 52.30 Expression 248.84 124.42 3.56 0.03* 0.09 0.64 Error (Expression) 2520.05 35.00 Group x Expression 115.11 28.78 0.82 0.52 0.04 0.25 Rise Time Group 441.86 220.93 1.32 0.28 0.07 0.27 Error (Group) 6027.03 167.42 Expression 39.20 19.60 0.18 0.84 0.01 0.08 Error (Expression) 7965.44 110.63 Group x Expression 266.03 66.51 Duration Group 416.46 208.23 0.35 0.71 0.02 0.10 Error (Group) 21469.64 596.38 Expression 1218.67 609.33 2.31 0.11 0.06 0.46 Error (Expression) 18977.13 263.57 Group x Expression 1172.87 293.22 1.11 0.36 0.06 0.33

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LIST OF REFERENCES Adelmann, P.K., & Zajonc, R.B. (1989). Facial efference and the e xperience of emotion. Annual Review of Psychology, 40, 249. Alexander, G.E., DeLong, M.R., & Strick, P.L. (1986). Parallel organi zation of functionally segregated circuits linking basal ganglia and cortex. Annual Review of Neuroscience 9, 357-381. Amick, M.M., Grace, J., & Chou, K.L. (2006). Body side of motor symptom onset in Parkinson's disease is associated with memory performance. Journal of the International Neuropsychological Society, 12 (5), 736-740. Antonini, A., Moeller, J.R., Nakamura, T., Spet sieris, P., Dhawan, V., & Eidelberg, D. (1998). The metabolic anatomy of tremor in Parkinson's disease. Neurology, 51 (3), 803-810. Barrick, T.R., Lawes, N., Mackay, C.E., & Clark, C.A. (2005). White matter pathway asymmetry underlies functional lateralization. Cerebral Cortex, 17(3), 591-598. Beck, A.T. (1978). Beck Depression Inventory San Antonio, TX: The Psychological Corporation. Blonder, L.X., Gur, R.E., & Gur, R.C. (1989a). Th e effects of right and left hemiparkinsonism on prosody. Brain and Language, 36(2), 193-207. Blonder, L.X., Gur, R.E., Gur, R.C., Saykin, A.J., & Hurtig H.I. (1989b). Neuropsychological functioning in hemiparkinsonism. Brain and Cognition, 9 (2), 244-257. Borod, J.C. (Ed.). (2000). Neuropsychology of emotion. New York: Oxford University Press. Borod, J.C. (1992). Interhemispheric and intrahemispheric control of emotion: A focus on unilateral brain damage. Journal of Consulting and Clinical Psychology, 60, 339-348. Borod, J.C., & Caron, H.S. (1980). Facedness and em otion related to lateral dominance, sex, and expression type. Neuropsychologia, 18(2) 237-241. Borod, J., Cicero, B., Obler, L., Welkowitz, J., Er han, H., Santschi, C., Grunwald, I., Agosti, R., & Whalen, J. (1998). Right hemisphere emotional perception: Evidence across multiple channels. Neuropsychology, 12, 446-458. Bowers, D., Bauer, RM, & Heilman, K. (1993). The nonverbal affect lexicon: Theoretical perspectives from neuropsychologica l studies of affect perception. Neuropsychology, 7(4) 433-444. Bowers, D., Miller, K., Bosch, W., Gokcay, D ., Pedraza, O., Springer, U., & Okun, M. (2006). Faces of emotion in Parkinsons disease: Micro-expressivity and bradykinesia during 54

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voluntary facial expressions. Journal of the International Neuropsychological Society 12(6), 765-773. Bowers, D., Bauer, D.M., Coslett, H.B., & Heilman, K.M. (1985). Processing of faces by patients with unilateral hemispheric lesions. I. Dissociation between judgments of facial affect and facial identity. Brain and Cognition, 4, 258-272. Bowers, D., Coslett, H.B., Bauer, R.M., Speedie, L.J., & Heilman, K.M. (1987). Comprehension of emotional prosody following unilateral hemi spheric lesions: processing defect versus distraction defect. Neuropsychologia, 25 (2), 317-328. Brodaty, H., Sachdev, P.S., Withall, A., Altendorf, A., Valenzuela, M.J., & Lorentz, L. (2005). Frequency and clinical, neuropsychologica l, and neuroimaging correlates of apathy following stroke--The Sydney Stroke Study. Psychological Medicine 35 (12), 1707-1716. Carroll, J., & McGinley, J. (2001) A screening form for identifyi ng mental health problems in alcohol/other drug dependent persons. Alcoholism Treatment Quarterly, 19 (4), 33. Coslett, H.B., & Heilman, K.M. (1989). Hemihypokinesia after right hemisphere stroke. Brain and Cognition, 9 (2), 267-278. Cubo, E., Bernard, B., Leurgans, S., & Raman, R. (2000). Cognitive and motor function in patients with Parkinsons disease with and without depression. Clinical Neuropharmacology 23(6), 331-334. Davidson, R.J. (1995). Cerebral asymmetry, emotion, and affective style. In R. J. Davidson & K. Hugdahl (Eds.), Brain asymmetry, (pp. 361). Cambridge, MA: MIT Press. Davidson, R.J. (2004). What does the prefrontal cortex do in affect: Perspectives on frontal EEG asymmetry research. Biological Psychology 67(1-2), 219-233. De Letter, M., Santens, P., & Van Borsel, J. (2 003). The effects of levo dopa on tongue strength and endurance in patients with Parkinson's disease. Acta Neurologica Belgica 103(1), 35-38. De Renzi, E., & Faglioni, P. (1965). The compar ative efficiency of intelligence and vigilance tests in detecting hemi spheric cerebral damage. Cortex, 1, 410-433. Djaldetti, R., Ziv, I., & Melamed, E. (2006). Th e mystery of motor asymmetry in Parkinson's disease. Lancet Neurology, 5 (9), 796-802. Ekman, P. (1992). Facial expressions of emotion: An old controve rsy and new findings. Philosophical Transactions of the Royal Society of London Series B: Biological Sciences. 335, 63. 55

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Fleminger, S. (1991). Left-sided Parkinson's di sease is associated with greater anxiety and depression. Psychological Medicine, 21 (3), 629-638. Geschwind, N. (1979). Specialization of the human brain. Scientific American, 241(3),180-199. Gainotti, G., Messerli, P., & Tissot, R. (1972). Qualitative analysis of unilateral spat ial neglect in relation to laterality of cerebral lesions. Journal of Neurology, Neurosurgery, and Psychiatry, 35 (4), 545-550. Goldstein, K. (1939). The organism: A holistic approach to biology derived from pathological data in man. New York: American Books. Harciarek, M., Heilman, K.M., & Jodzio K. (2006) Defective comprehension of emotional faces and prosody as a result of right hemisphere stroke: Modality versus emotion-type specificity. Journal of the Inte rnational Neuropsyc holgocial Society, 12 (6), 774-81. Heilman, K.M., Blonder, L.X., Bowers, D., & Valenstein, E. (2003). Emotional disorders associated with neurological diseases. In K.M. Heilman & E. Valenstein (Eds.), Clinical neuropsychology ( 4th ed. pp. 447-477). New York: Oxford University Press. Heilman, K.M., & Bowers, D. (1990). Neuropsychol ogical studies of emo tional changes induced by right and left hemispheric st udies. In N.L. Stein, B. Leventhal, & T. Trabasso (Eds.), Psychological and biological approaches to emotion (pp. 97-113). Hillsdale, NJ: Erlbaum. Heilman, K.M., Watson, R.T., & Valenstein, E. ( 2003). Neglect and related disorders. In K.M. Heilman & E. Valenstein (Eds.), Clinical neuropsychology ( 4th ed., pp. 296-342). New York: Oxford University Press. Howes, D., & Boller, F. (1975). Simple react ion time: evidence for focal impairment from lesions of the right hemisphere. Brain, 98 (2), 317-332. Hughes, A.J., Daniel, S.E., Kilford, L., & Lees, A. J., (1992). Accuracy of clinical diagnosis of idiopathic Parkinsons disease: A clinico-pathological study of 100 cases. Journal of Neurology, Neurosurgery, and Psychiatry 72 (6), 701-707. Katzen, H.L., Levin, B.E., & Weiner, W. (2006). Side and type of motor symptoms influence cognition in Parkinsons disease. Movement Disorders, 21 (11), 1947-1953. Kempster, P.A., Gibb, W.R., Stern, G.M., & Lees, A.J. (1989). Asymmetry of substantia nigra neuronal loss in Parkinson's disease and its relevance to the mechanism of levodopa related motor fluctuations. Journal of Neurology, Neurosurgery, and Psychiatry 52 (1), 72-76. Kirsch-Darrow, L., Fernandez, H.F., Marsiske, M., Okun, M.S., & Bowers, D. (2006). Dissociating apathy and depressi on in Parkinsons disease. Neurology 67, 33-38. 56

PAGE 57

Lang, A.E., & Fahn, S. (1989). Assessment of Park insons disease. In T.L. Munsat (Ed.), Quantification of neurologic deficit (pp. 285-309). Boston, MA: Buttersworths. Lee, C.S., Schulzer, M., Mak, E., Hammerstad, J.P ., Calne, S., & Calne, D.B. (1995). Patterns of asymmetry do not change over th e course of idiopathic park insonism: Implications for pathogenesis. Neurology, 45 (3) 435-439. Lee, T.W., Josephs, O., Dolan, R.J. & Critchley, H.D. (2006). Imitating expressions: Emotionspecific neural substrates in facial mimicry. Social Cognitive and Affective Neuroscience, 1(2), 122-135. Levy, R., & Dubois, B. (2006). Apathy and the functi onal anatomy of the prefrontal cortex-basal ganglia circuits. Cerebral Cortex, 16 (7), 916-928. Lieberman, A. (2006). Depression in Parkinson's disease--A review. Acta Neurologica Scandinavica, 113 (1), 1-8. Liotti, M., & Tucker, D. M. (1995). Emotion in asymmetric cortico-limbic networks. In R. J. Davidson & K. Hugdahl (Eds.), Brain Asymmetry (pp. 389). Cambridge, MA: MIT Press. Lozza, C., Mari, R.M., & Baron, J.C. (2002). Th e metabolic substrates of bradykinesia and tremor in uncomplicated Parkinsons disease. Neuroimage, 17(2), 688-699. Marin, R.S. (1991). Apathy: A neuropsychiatric syndrome. Journal of Neuropsychiatry and Clinical Neuroscience, 3, 243-254. Mark, M.A., & Mark, M.H. (1994). Parkinsons disease and depression: The relationship to disability and personality. Journal of Neuropsychiatry and Clinical Neuroscience, 6 (2), 165-169. Mattis, S. (2001). Dementia Rating Scale-2. Odessa, FL: Psychological Assessment Resources. McDonald, W.M., Richard, I.H., & DeLong, M.R. (2003). Prevalence, etiology, and treatment of depression in Parkinsons disease. Biological Psychiatry, 54 (3), 363-375. Meador, K.J., Loring, D.W., Lee, G.P., Brooks, B. S., Nichols, F.T., Thompson, E.E., Thompson, W.O., & Heilman, K.M. (1989). Hemisphere asymmetry for eye gaze mechanisms. Brain, 112(1), 103-111. Obeso, J.A., Rodriguez-Oroz, M.C., Rodriguez, M., Arbizu, J., & Gimenez-Amaya, J.M. (2002). The basal ganglia and disorders of movement: Pathophysiological mechanisms. News in Physiological Sciences, 17, 51-55. 57

PAGE 58

Papez, J.W. (1995). A proposed mechanism of emotion. 1937. Journal of Neuropsychiatry and Clinical Neuroscience, 7 (1), 103-112. Pentland, B., Gray, J.M., Riddle, W.J., & Pitc airn, T.K. (1988). The effects of reduced nonverbal communication in Parkinson's disease. The British Journal of Disorders of Communication, 23 (1), 31-34. Petit, L., Simon, G., Joliot, M., Andersson, F ., Bertin, T., Zago, L., Mellet, E., & TzourioMazoyer, N. (2007). Right hemisphere dom inance for auditory attention and its modulation by eye position: An event related fMRI study. Restorative Neurology and Neuroscience, 25 (3-4), 211-225. Phan, K.L., Wager, T., Taylor, S.F., & Liberzon, I. (2002). Functional neuroanatomy of emotion: A meta-analysis of emotion activ ation studies in PET and fMRI. Neuroimage, 16, 331348. Rabinstein, A.A., & Shulman, L.M. (2001). Management of behavioral and psychiatric problems in Parkinsons disease. Parkinsonism and Related Disorders, 7, 41-50. Rinn, W.E. (1984). The neuropsychol ogy of facial expression: A revi ew of the neurological and psychological mechanisms for producing facial expressions. Psychological Bulletin, 95(1), 52-77. Spicer, K.B., Roberts, R.J., & LeWitt, P.A. (1988). Neuropsychological performance in lateralized parkinsonism. Archives of Neurology, 45, 429-32. St. Clair, J., Borod, J.C., Sliwinski, M., Cote L.J., & Stern, Y. (1998). Cognitive and affective functioning in Parkinsons disease patie nts with lateralized motor signs. Journal of Clinical and Experimental Neuropsychology, 20 (3), 320-327. Semmes, J. (1968). Hemispheric specializat ion: A possible clue to mechanism. Neuropsychologia, 6, 11-26. Simons, G., Smith Pasqualini, M.C., Re ddy, V., & Wood, J. (2004). Emotional and nonemotional facial expressions in people with Parkinsons disease. Journal of the International Neurops ychological Society 10, 521-535. Starkstein, S.E., Mayberg, H.S., Preziosi, T.J ., Andrezejewski, P., Leiguarda, R., & Robinson, R.G. (1992). Reliability, validity, and clinical correlates of ap athy in Parkinson's disease. The Journal of Neuropsychiatry and Clinical Neurosciences, 4 (2), 134-139. Starkstein, S.E., Robinson, R.G., & Price, T.R. (1987). Comparison of cortical and subcortical lesions in the production of poststroke mood disorders. Brain, 110(4), 1045-1059. Stevens, M.C., Calhoun, V.D., & Kiehl, K.A. (2005). Hemispheric differences in hemodynamics elicited by auditory oddball stimuli. Neuroimage, 26(3), 782-792. 58

PAGE 59

59 Stuss, D.T., Guberman, A., Nelson, R., & Laro chelle S. (1988). The neuropsychology of paramedian thalamic infarction. Brain and Cognition, 8 (3), 348-378. Teuber, H.L. (1955). Physiological psychology. Annual Review of Psychology, 6, 267-296. Tucker, D.M. (1991). Development of emotion and cortical networks. In M. Gunnar & C. Nelson (Eds.), Minnesota symposium on child development: Developmental neuroscience. New York, NY: Oxford University Press. Tomer, R., Levin, B.E., & Weiner, W.J. (1993). Side of onset of motor symptoms influences cognition in Parkinson's disease. Annals of Neurology, 34 (4), 579-84. Turner, R.S., Grafton, S.T., McIntosh, A.R., DeLong, M.R., & Hoffman J.M. (2003). The functional anatomy of park insonian bradykinesia. Neuroimage 19(1), 163-179. Weintraub, D., Moberg, P.J., & Duda, J.E. (2004 ). Effect of psychiat ric and other nonmotor symptoms on disability in Parkinson's disease. Journal of the American Geriatrics Society, 52 (5), 784-788. Weintraub, D., Moberg, P.J., Duda, J.E., Katz I.R., & Stern, M.B. (2003). Recognition and treatment of depression in Parkinson's disease. Journal of Geriatric Psychiatry and Neurology, 16 (3), 178-183. Wooten, G.F., Currie, L.J., Bovbjerg, V.E., Lee, J. K., & Patrie, J. (2004). Are men at greater risk for Parkinson's disease than women? Journal of Neurology Neur osurgery and Psychiatry, 75(4), 637-639. Yu, H., Sternad, D., Corcos, D.M., & Vaillancourt D.E. (2007). Role of hyperactive cerebellum and motor cortex in Parkinson's disease. Neuroimage, 35(1), 222-233. Zetusky, W.J., & Jankovic, J. (1985). Laterality and symptom association in Parkinson's disease. Archives of Neurology, 42 (12), 1132-1133.

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BIOGRAPHICAL SKETCH Anne Noelle Nisenzon is originally from V oorhees, NJ, and graduated Summa Cum Laude from Boston University with a Bachelor of Arts in psycholo gy. Prior to entering graduate school, she obtained functional neuroimaging research experience at Massachusetts General Hospital in Boston, MA. She is currently pursui ng her doctoral degree in clinical psychology at the University of Florida. Current research and clinical interests include the emotional aspects of Parkinsons disease with a focu s on patient-centered outcomes related to deep brain stimulation treatment. 60