THE NUTRITION AND PHYSICAL ASSESSMENT OF PATIENTS WITH NEUROLOGICAL DISORDERS

Objective: To describe cognitive, nutritional and physical functioning status of those with diagnosed neurological disorders for at least one year. Design: This is a cross-sectional study. Setting: University of Rhode Island’s Speech and Hearing Clinic. Participants: Community-dwelling adults living with Parkinson’s disease (PD) or acquired brain injury (ABI) for >12 months. Main Outcome Measure(s): Cognitive-linguistic status was measured via the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). Nutritional and cardio-metabolic status were measured using the dietary screening tool (DST), anthropometrics (height, weight, body mass index (BMI), body composition), biochemical (lipid and glucose profile), and clinical (blood pressure) measures. Physical activity and functioning were measured via the Physical Activity and Disability Survey (PADS), short physical performance battery (SPPB), and the timed up and go (TUG) test. Results: Twelve participants were assessed (8 PD, 4 ABI). Participants with PD had significantly higher total RBANS scores than participants with ABI (87.1±14.6 vs. 66.0±12.6, p=0.034, d=2.455). Mean BMI (n=12) was 26.8±3.0kg/m and the majority of participants were overweight. DST scores indicated 58% (N=7) at possible nutrition risk and 25% (N=3) were at nutrition risk. Mean PADS scores (94.9±89.7) indicated participants were physically active. A positive correlation was found between general activity scores and DST scores (r=0.697, p=0.012). Fifty percent of participants reported suboptimal SPPB, balance or TUG scores. Multiple risk factors for development of CVD were present in all participants. Conclusion: Deficits in cognition, low dietary quality and physical functioning, and cardio-metabolic risk factors are frequently reported in patients with neurological disorders. These findings confirmed the presence of cognitive, dietary and physical decline in our participant group and support the need for an interdisciplinary team to work with patients and caregivers to improve health and prevent further development of comorbidities in this population.


LIST OF TABLES
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INTRODUCTION
Parkinson's disease (PD), traumatic brain injury (TBI), and stroke are neurological disorders that can result in lifelong challenges that impact cognitive, physical, and psychosocial functioning [1][2][3][4][5] , which, in turn, can jeopardize dietary intake and increase likelihood of nutritional risk and cardiovascular disease (CVD).
Parkinson's disease is a progressive, neurodegenerative, movement disorder affecting nearly one million people in the United States 6 . Traumatic brain injury and stroke are types of acquired brain injury (ABI), defined as structural damage to the brain 7,8 .
Nearly 2,500,000 people experience a TBI or stroke annually in the United States 8,9 .
While these neurological diseases are each unique and have different long-term effects, they share similar complications that can negatively impact nutritional status and dietary intake, as well as physical function.
Limited research exists examining the interaction between cognition, nutritional status, and physical function for those with PD and ABI one year or more after diagnosis. Unintentional weight loss is typical at the time of PD diagnosis and nutritional status declines as the disease progresses 1 . Malnutrition and muscle wasting are consistently reported in the acute stages of ABI [10][11][12][13] . Since nutritional status is compromised in the acute phase after an ABI, long-term nutritional status is likely to be poor 13 . However, due to a scarcity of research, little is known about the long-term nutritional status of those with ABI. Cognitive and physical impairment associated with these neurological disorders may contribute to metabolic and nutritional imbalances 1,3,5,14,15 . 7

Assessment Visit and Data Collection
Anthropometrics Height (cm) and weight (kg) were measured using a stadiometer (Webb City Missouri). Height was rounded to the nearest 0.5 cm and weight was rounded to the closest 0.1 kg. Height and weight were used to calculate BMI (kg of body weight/height in meters 2 ). Predetermined categories classified BMI scores: underweight <18.5 kg/m 2 , normal weight = 18.5-24.9 kg/m 2 , overweight = 25-29.9 kg/m 2 and obese ≥ 30 kg/m 2 22 . A foot-to-foot bioelectrical impedance analysis device (Tanita BF-556, Arlington Heights Illinois) was used to obtain body composition and report percent (%) body fat. American Council on Exercise 23 , any female with ≥32% body fat and any male with ≥25% body fat was considered obese.

Clinical
Blood pressure was measured after participants sat quietly for five minutes using an automatic blood pressure machine (Omron Healthcare Inc., Bannockburin Illinois). Systolic blood pressure (SBP) <120 mmHg and diastolic blood pressure (DBP) <80 mmHg was considered optimal. Systolic blood pressure >130 mmHg and 8 DBP >85 mmHg was borderline high, while SBP > 140 mmHg and DBP >90 mmHg was considered hypertensive.

Cognitive Linguistic
Cognitive-linguistic function was assessed using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) 25 . The RBANS includes 12 subtests, with five index scores, summarizing: immediate memory, visuospatial/constructional, language, attention and delayed memory. The total score is the sum of the five index scores. Scoring is based on a standardized mean of 100 and a standard deviation of 15; a score <70 indicates suboptimal cognitive function.

Swallowing Evaluation
The Swallowing SWAL-QOL is a 44-item survey where participants rate factors about 10 quality of life concepts related to swallowing, primarily in regards to eating and diet 26,27 . The highest possible score is 220, the higher the score the better one's swallowing function.

Dietary Intake and Nutritional Risk Assessment
The Dietary Screening Tool (DST) is a 25-item questionnaire that is used to identify dietary patterns and nutritional risk in older adults 28,29 . Participants reported how frequently they consumed a food or type of food. A composite score was calculated based on subcomponents of the DST. The sub-components and point distribution included: whole fruit and juices (15 points), vegetables (15 points), lean proteins (10 points), added fats, sugars and sweets (25 points), dairy (10 points) and processed meats (10 points), and use of a dietary supplement (5 points).

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These sum-components are composited and total scores are defined for three different nutritional risk levels: (<60) at risk, (60)(61)(62)(63)(64)(65)(66)(67)(68)(69)(70)(71)(72)(73)(74)(75) possible risk, and (>75) not at risk 28 . Categorization into three nutritional risk categories provides a way to determine if a patient needs a follow-up or nutrition assessment 28 . The DST Dietary intake was broken down based on point classification for the DST sub-components 28 to explore specific areas contributing to low dietary quality. These sub-components were created to identify specific areas of the diet that may be problematic on an individual basis 28 .
Participants with fewer than 50% of total possible points for each subcomponent and if the participant did not currently take dietary supplement were considered low sub-scores. Less than 50% was selected as an exploratory marker to indicate infrequent/inadequate intake of whole grains, fruits, vegetables, dairy or lean proteins, and high consumption of processed meats, added sugars, fats and sweets.

Physical Activity and Functioning
The Physical Activity and Disability Survey (PADS) 30,31 was used to assess physical activity levels. It covers a wide range of activities and includes six subscores: exercise, leisure-time physical activity (LTPA), general activity, therapy, employment, and wheelchair use. The PADS is coded based on intensity, type and amount of activity and can detect varying levels of physical activity 32 . Raw scores of <27 indicate minimal, 28-42 is minimal to moderate, 43-67 is moderate, and > 68 indicates a high activity 30 .
The short physical performance battery (SPPB) 33 was completed to assess participants' global physical functioning and included usual gait speed, standing balance tests, and five repeated chair stands. SPPB scores are on a 12 point scale, the higher the score the better physical function. Scores 8-12 are considered "high functioning 33 ." A timed up and go (TUG) test was used to assess basic functional mobility 34 .
It measures the time it takes for the participant to rise from a chair, walk three meters, turn around and walk back to the chair. Time was recorded in seconds, and the shorter amount of time, the better the score. The test was administered twice and the better score was recorded. A TUG score >13.5 is considered high risk for falls 35

Other Questionnaires
A non-validated medical history questionnaire was be used to identify healthrelated conditions and how these conditions may impact health.

Cardio-Metabolic Assessment
Cardiovascular disease is the disease of the heart and/or blood vessels 36 .
Traditional risk factors for CVD include modifiable and non-modifiable risk factors.
Non-modifiable risk factors include age, sex and ethnicity. Modifiable risk factors include being overweight/obese, having hypertension, elevated blood glucose levels, and dyslipidemia 37 . As well lifestyle factors such as physical inactivity, tobacco use and a diet high in saturated fat and processed foods and low in fruits and vegetables and fiber 37,38 .
Those living with neurological disorders suffer physical and cognitive impairment that may disrupt activities of daily living (ADL); as a result physical barriers (such as partial or no use of arms and legs, as well as use of an assistive device) were examined due to the possibility they may promote a sedentary lifestyle. Cognitive function was also included as a CVD risk factor through examining total RBANS scores and three RBANS index scores (immediate memory, attention, delayed memory) <70.

Statistical Analysis
Statistical analysis were not hypothesis driven, but conducted to generate hypotheses and explore the population. Data were analyzed using SPSS, version 22.0 for Windows (IBM Corp. Summers, NY). Descriptive statistics were conducted and distribution of data was assessed through analyzing skewness and kurtosis. For data that were not normally distributed, proper statistical methods were used to account for this. Categorical variables are represented as numbers and percentages and continuous variables are reported as mean ± standard deviation.
To analyze CVD risk factors, the participants were individually analyzed across the eight categories. The most frequent risk factors were then analyzed based on the variables within the eight CVD categories and reported as top CVD risk factors.
For normally distributed data, independent t-tests were conducted to determine if there were significant differences between groups regarding assessment variables.
Cohen's d was calculated to describe effect size for differences between groups in 12 normally distributed variables (0.2 = small effect, 0.5 = medium effect, 0.8 = large effect). For data not normally distributed, Mann-Whitney U tests were used to analyze differences between groups and effect size was signified through calculating r (0.1=small effect, 0.3=medium effect, 0.5=large effect). Differences between groups for categorical variables were identified using Fisher Exact Tests. Phi squared or Cramer's V were used to signify effect size (0.1=small effect, 0.3=medium effect, 0.5=large effect). Pearson's R correlations were used with normally distributed variables, and Spearman Rho correlations were used as the non-parametric alternative.
Differences between groups were significant when p=<0.05.

RESULTS
Demographic characteristics and results from specific assessment measures are summarized in Table 1. Of the four ABI participants two were diagnosed with stroke, one with a TBI and one participant had a diagnosis of TBI and stroke. An independent t-test found, those living with ABI were diagnosed significantly longer than those living with PD (p=0.01, d=1.8 No significant correlation was found between RBANS scores and nutrition, cardio-metabolic, or physical assessments. As indicated by DST scores, three participants with PD were classified at nutritional risk and seven participants (4 PD and 3 ABI) were classified at possible nutrition risk (Table 2). Two participants with PD reported diet changes to soft, easy to chew foods, while all other participants reported to follow a "full normal diet," not modified in texture or consistency. All participants reported drinking thin liquids without any modifications.
Results from 10 DST sub-scores per participant are described in Table 3 Table 4. Six participants had partial use of arms and eight had partial use of legs, while seven participants reported to use an assistive device.
The range of PADS scores for participants ranged from -12 to 311. Mean total TUG score was 12.1±3.2 seconds. Physical barriers, physical activity level and physical functioning for each participated are reported in Table 4.
The secondary aim of this study was to analyze how compromised cognition, nutrition, and physical activity and functioning may increase CVD risk. Seven participants were taking medication to manage blood pressure and/or lipid profiles.
Results of the RBANS revealed that three participants had total index scores <70 (1 PD, 2 ABI), three participants (1 PD, 2 ABI) had <70 Immediate Memory Scores, three ABI participants had <70 Attention scores and two PD and one ABI had <70 delayed memory scores. In total, five participants had cognitive impairment in one of these four areas. Typically, cognitive status is not classified as a CVD risk factor, however these tests have been included to explore the potential impact of impaired cognition associated with neurological disorders may have on CVD risk. Additionally, the presence of possible nutrition risk (Table 3) and compromised physical functioning ( Low DST and general activity scores and their relationship suggests further investigation of disease-related eating barriers, such as ability to buy and prepare meals 5,14,43 . Altered satiety cues and change in appetite associated with TBI may also be present 3,42 . It also implies isolated activity time is less of a barrier than performing household tasks. Most participants were married or lived with family, and household work was performed by someone else. These findings are consistent with past research, which found 86% of those with PD were disabled from participating in ADL, but 88.8% had social support, and 64% participated in regular exercise/leisure time activity 44 . Future physical activity interventions should target ways to help increase the ability to independently carry out more ADL, which may improve diet quality.

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Evidence shows physical activity can help reduce age-related physical and cognitive decline [45][46][47] . The presence of elevated exercise and LTPA activity and their correlation with SPPB scores may imply a protective effect of activity on participant's physical decline and should be examined over the next five years.
Due to the small sample size and the use of pharmacological medications to manage blood pressure and/or cholesterol levels by many participants (58.3%), it is hard to speculate the risk factor with the biggest impact on the development of a cardiovascular event in those with neurological disorders. Despite the use of medication to manage lipid profiles and blood pressure, other CVD risk factors were still present and may lead to a CVD event. This can be highlighted by presence of elevated bodyweight and low dietary scores in many participants and shows the importance to continue to monitor and promote heart health in this population.
Research still needs to better understand the risk of CVD in those with PD and whether these is in fact a protective cardio-metabolic effect present in those with PD or an increased risk of a CVD event [16][17][18]48,49 Total RF  6  8  7  3  3  3  5  7  2  3  4 Check marks indicate participants are at risk of poor physical function and activity level. Portray poor physical function and activity level. Physical barriers include if participant has partial use of arms or legs, uses an assistive device, and reports frequent falls. † Indicates PPT does not participate in PADS sub-scores (exercise, leisure time, or general activity) and received a score of 0 or below. Abbreviations: PPT, participant; LTPA, Leisure-Time Physical Activity; RF, risk factor

I. Introduction
Parkinson's disease (PD), traumatic brain injury (TBI), and stroke are neurological conditions that can result in lifelong challenges that affect physical, cognitive and psychosocial functioning [1][2][3][4][5] , which in turn can jeopardize dietary intake and increase likelihood of nutritional and cardiovascular disease (CVD) risk. Traumatic brain injury and stroke are subtypes of acquired brain injury (ABI), a term used to describe structural damage to the brain 6,7 . Approximately 1,700,000 and 795,000 people experience a TBI or stroke, respectively, every year in the United States (US) 7,8 .
Parkinson's disease is a progressive, neurodegenerative, movement disorder that one million people in the US live with 9 . While these neurological diseases are each unique and have different long-term impacts, they have similar complications that can negatively impact nutritional status and dietary intake 1,3,10 .
Limited research exists examining the relationship between cognition, nutrition and physical activity in those with one of these neurological disorders. Research has examined long-term (a year or more following diagnosis) nutritional status of those living with PD 1,11,12 . Unintentional weight loss is typical at the time of PD diagnosis and nutritional status declines as the disease progresses 1 . Meanwhile, nutritional status of patients in the acute stages of stroke and TBI has been assessed and malnutrition and muscle wasting are consistently reported [13][14][15][16] . Evidence indicates up to six months following a stroke and two months following a TBI are a high-risk time for malnutrition 5,17 , however very little research has examined nutritional status a year after. Since nutritional status is compromised in the acute phase after an ABI, long-term nutritional status is likely to be poor 16 . In addition to risk of poor nutritional status, physical disabilities associated with these neurological disorders 3,18,19,20 warrant an assessment of physical activity and functioning. An assessment of both nutrition and physical activity will provide a clearer idea of if these neurological disorders are at increased risk of diet and exercise related comorbidities.
Research indicates there may be a protective cardio-metabolic effect of PD, even in those with PD that are overweight 21,22 . Meanwhile, those with TBI are at increased risk for significant weight change, as well diseases related to physical activity and diet, such as coronary heart disease (CHD) and metabolic syndrome, a disease marked by abdominal obesity, hypertension, dyslipidemia and insulin resistance 3,23 . Research indicates an obesity paradox seems to exist following stroke, decreasing risk of reoccurring stroke 15,24 , however a cardiovascular risk assessment of those living with stroke has not been completed.
Due to complications of neurological disorders, it is implied that nutritional imbalances can result in over-nutrition or under-nutrition 1,3,5,17,23 . While research has examined nutritional status in those with PD, limited research exists analyzing how cognition, nutrition and physical activity and functioning relate. Similar complications of these three disease states suggest research should examine long-term nutritional status of those with stroke and TBI, as well as cognition and physical activity. Due to this lack of research, a cross-sectional study including those living with PD, TBI and stroke is necessary to assess dietary quality, nutritional status, physical activity and physical functioning, as well as cardiovascular risk, and quality of life.

The Definition, Prevalence and Effects of PD
Parkinson's Disease is a neurodegenerative, movement disorder caused by the death of dopamine cells 9 . Dopamine cells are the neurons that regulate motor function 25 and are concentrated in the substantia nigra, the area of the brain that controls movement 26 . In addition to motor symptoms (partial or full functional loss of a body part), those living with PD experience a variety of cognitive deficits, even during early stages of the disease 27  Parkinson's can be classified into a variety of different subtypes, usually based upon the dominant motor symptoms present. Parkinson's can also be identified in stages based on the Hoehn and Yahr scale (HY) 34 . This one through five scale was developed to describe degree of disability and functional limitations related to PD 34 .
Phase one describes early onset symptoms, while stage five would describe the final phases, where one is confined to a wheelchair or bed. The progression of the disease is usually marked by increased motor impairment 9 . These motor symptoms, as well as, non-motor symptoms, can impact dietary intake and compromise nutritional status 35,36 .
Non-motor symptoms prevalent in PD include: cognitive impairment, neuropsychiatric symptoms, sleep disturbances, fatigue, gastrointestinal symptoms and sensory disturbances 37,38 . Cognitive dysfunction can occur early in diagnosis 39 .

Parkinson's Disease and Effects on Cognition
Parkinson's disease is associated with a variety of cognitive deficits that appear in the earliest stages of the disease and continue to worsen as the disease progresses 27,37,38 . Within 15 years of diagnosis, over 80% of those living with PD experience a form of cognitive impairment (deficiency in brain function that affects memory, language, perception, visuospatial aspects, ability to carry out tasks and judgment) 40 or dementia 41 . These alterations can interfere with everyday functioning 27 .
Older age at disease onset, depression, male gender, severity of motor symptoms and advanced disease stage are risk factors for the development of mild cognitive impairment (MCI) for those with PD 10 . Evidence of MCI in the early stages of PD is associated with the incidence of dementia in later stages of PD 42 .
Cognitive symptoms associated with PD are mostly a result of the pathological changes within the brain, including changes in the dopaminergic pathway 43 .
Dopaminergic drugs, such s levodopa (L-dopa), used to synthetically produce 37 dopamine have been associated with improving cognition in PD patients, as well as negatively impacting cognition 44,45 . There are multiple reasons for cognitive changes in those with PD and many pathways are disrupted as a result of lack of dopamine deficiency. In addition to lack of dopamine, the presence of Lewy body production (abnormal aggregates of protein that develop inside nerve cells and interfere with signal conduction) and cell loss in the brain can also disrupt cognitive function 39,46 .
In those newly diagnosed with PD, the most prominent cognitive issues are related to memory and executive functions (EF) 47 . Executive function is the set of mental processes that help one connect past experience with present action 48 . Deficits with EF include difficulty with concept formation, decision-making, cognitive flexibility and selective attention 37,47,49 . Difficulties with EF can be attributed to damage of the frontal cortex as a result of PD 47,49 . A cross-sectional study examining the pattern of EF in 34 participants with mild to moderate PD, with a mean duration of 68.2±52.4 months, found nearly 45% of participants had a degree of EF impairment 49 .
Those living with PD have issues with dual-tasking, which are tasks that require simultaneous performance of at least two cognitive functions along with motor functions 43 . Wild and colleagues 27 examined dual tasking, in those with PD (n=18) versus healthy older adults (n = 18) and found that those with PD compromised the cognitive function tasks to focus on the motor task 27 . Poor dual tasking is also an indicator of impaired EF. These symptoms may contribute to a compromised quality of life and health status 39,47 , which in turn may impact one's ability to make proper dietary choices.

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In addition to compromised EF and memory, neuropsychiatric conditions, including depression, anxiety and apathy, often precede motor symptoms 50 . These conditions add significant burden to PD 43 and impact quality of life 51 . Paranoid delusions, hallucinations, impulse control disorder, and addictive symptoms can result due to treatment and medications for PD 43 . These cognitive and neuropsychiatric impairments, combined with motor impairment, not only impact quality of life but have physiological side effects on the body that impact energy needs 1 .

Physiological Side Effects and Energy Needs of PD
Physiological side effects and energy needs vary depending on the stage of the disease 1,52 Unintentional weight loss preceding a PD diagnosis is common 53 , and weight then tends to increase immediately after diagnosis when treatment is initiated 1,52 . The initial pre-diagnosis weight loss is attributed to the energy imbalance from the increase in energy expenditure as a result of motor symptoms, such as rigidity and dyskinesias (involuntary muscle movements) compared to reduced energy intake. A longitudinal, prospective study examined weight changes of 468 people with PD and found a mean weight loss of 5.2 pounds 10 years preceding diagnosis, but a fairly constant weight two to four years prior to diagnosis 53

Malnutrition and PD: Under-nutrition
Malnutrition, or poor nutritional status, is defined as an imbalance of energy, macronutrients and/or micronutrients that results in compromised body shape, size and composition, function and clinical outcomes 55 . It includes under-nutrition, which results from insufficient intake to meet energy expenditure 56 , and over-nutrition, which is caused by excessive calorie intake and/or inadequate activity 56 . Proteinenergy malnutrition refers specifically to deficiency rather than an excess of protein and energy 36 . It also can result in a lower quality of life and poorer health outcomes, which in turn can increase risk of falls, hospitalization and admittance to aged care facilities 36,57,58 . Assessments of nutritional status determine if one is malnourished through examining anthropometrics, biochemical and clinical data, and dietary intake.
Nutrition assessments of those living with PD typically find compromised nutritional status 11,12,59 .
The average age of those diagnosed with PD is 60 years old 60 . Change in weight, particularly weight loss, during aging is typical 61 , yet it seems to be greater in those with PD 62 . Changed in total body weight in men and woman overtime varies.
Typically, men gain weight until about the age of 55 and women until the age of 65; after this point in time weight loss is common. Weight loss in healthy aging adults occurs because of the loss of lean muscle tissue, which is replaced with fat 61 .
Under-nutrition is prevalent in those living with PD 11,12,59 , however it is difficult to determine how much of it is due to PD 36 . The majority of PD patients are elderly and as a result are also experiencing physiological changes associated with aging 61 . In addition to weight loss, changes include reduction of digestive secretions, intestinal absorption, protein synthesis, and factors that decrease energy intake 63 ; these factors include altered sense of smell and taste, loss of teeth and ill-fitting dental prostheses 63 . A mean weight loss of 7.7 pounds during the 8 years following diagnosis of PD has been reported 53 . The study found energy intake to be similar between those with PD and those without PD shortly before diagnosis, but saw an increase in energy intake shortly after the diagnosis of PD 53 . This research implies that weight loss associated with PD can be due to an increase in energy expenditure unique to PD, that healthy adults to do not experience 53 .
Compared to age matched controls, research has found lower body mass index (BMI) scores in those with PD 64 . Other study have also found those with PD to have significantly lower BMI scores (24.4±0.5 kg/m 2 ) and percent body fat (%BF) (22.2%±0.9) compared to age-matched controls without PD (26.3±0.4 kg/m 2 , 24.6%±0.9) 62 . The majority of these participants were in stage two of PD 34,62 .
Motor and non-motor symptoms 1,36 often compromise dietary intake in those living with PD 36,59 and may also impact malnutrition. As PD progresses, a decreased response to treatment occurs and motor control declines 1,65 . Decline in motor control, such as the presence of dyskinesia and rigidity raises energy expenditure and can lead to negative energy balance and weight loss 1 . Physical changes and motor symptoms such as curve posture, shuffling gait and postural instability 1 make buying, preparing and eating food independently difficult 1,35,66 . This development of chronic disabilities can interfere with activities of daily living (ADL), which include washing, dressing, eating and walking 58 . Those with PD lose the ability to eat independently due to decreased hand-mouth coordination and decline in fine movements to use utensils 30,67 .
Motor symptoms can lead to a reduction in energy intake and weight 1,66 .
Non-motor symptoms can also cause a decline in dietary intake 36 and includes depression, dementia, confusion, and apathy, as well as gastrointestinal symptoms; typical gastrointestinal symptoms include constipation, dysphagia (difficulty swallowing), early satiety, decreased gastric transit time, nausea, change in taste, loss of appetite and sialorrhea (excessive drooling), also cause a decline in dietary intake 1,36,68,69 . A qualitative study examined food shopping, cooking and eating habits in older women with PD, and found decrease in sense of smell, appetite and taste in combination with issues transporting food to the mouth and swallowing were major issues associated with altering nutritional status 70 . Due to these barriers to meet nutrient and energy needs, those with PD are at increased for weight loss and loss of lean body mass 36 . Weight loss is a natural part of the aging process, yet seems to be more common and severe in those with PD 62 .
Research indicates lower body weight and barriers for inadequate dietary intake in this population, indicating under-nutrition is present in this population.
Findings reveal a strong correlation between lower Mini Nutritional Assessment (MNA) scores and time since PD diagnosis 65 . A cross-sectional, population-based study, which included 135 PD cases in two regions of North East England, found that 21 of the 135 (15.4%) participants were classified as malnourished 11 . The study also found that females with PD, were more likely to be severely malnourished (BMI <18.5) than male counterparts 11 ; this research is consistent to males and females without PD 71 . Due to the larger BMI scores and waist circumference in malnourished men with PD, accompanied by the presence of muscle wasting, these malnourished participants are likely suffer from sarcopenic obesity, while malnourished females may suffer from both muscle and fat loss 12 . Sarcopenia is the age-related loss of lean muscle mass and muscle function [73][74][75] . These results indicate that nutritional assessments for those living with PD are necessary. More research is needed to understand exactly why malnutrition occurs in this population and to help prevent malnutrition and sarcopenia, as well as to monitor how medications and treatment impact weight in this population.
Medications and treatment for PD may also impact weight and food choices 1,64,76 . Dopaminergic treatment has been associated with a decrease in weight for those with PD who experience dyskinesia, common complication of L-dopa 64 .
Lower BMI scores are associated with advanced PD patients taking higher dosages of L-dopa 64 . A common side effect of L-dopa is nausea and vomiting, to help limit this prescribed with carbidopa as to reduce symptoms of nausea and vomiting and help control PD symptoms. Reducing symptoms of nausea and vomiting, as well as seeking alternative treatments may help those with PD reduce risk of weight loss While undernutrition and weight loss are problematic for those with PD, weight gain can also occur and is associated with PD treatment 1 .

Malnutrition and PD: Over-nutrition
Time of PD diagnosis is often associated with weight gain, because those living with PD begin treatment to control symptoms that promote weight loss 1 . While some research has found weight loss in response to treatment for PD, other research has reported weight gain as a result. For instance, surgical procedures to treat PD, such as deep brain stimulation (DBS) are associated with significant weight gain 52,77 .

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Pharmacological medications can also cause weight gain 52,76 . Dopamine agonists are medications that stimulate the parts of brain to believe it is receiving dopamine. Since they are not as potent as L-dopa, they are less likely to cause dyskinesia 78 , which in turn would decrease energy expenditure associated with dyskinesia. They also can cause compulsive behaviors, include compulsive eating and undesirable weight gain 76 . In a report by Nirenberg and Waters 76 , seven cases of PD are described that experienced compulsive eating and undesired weight gain related to dopamine agonists, these participants saw an average 15% increase (13 kg ± 7 kg) in body weight. Five of the seven participants decreased or discontinued dopamine agonists and self-reported a decrease in food cravings and weight 76 . Despite a small sample size findings suggest further research should evaluate the impact of dopamine agonists, weight status and dietary habits on those living with PD.
Another treatment that impacts weight is DBS, a surgical option for those with PD, and utilized by approximately 30,000 people with PD worldwide 79 . In this surgical procedure, an impulse generator is placed under the collarbone that provides an electrical impulse to the substantia nigra 79 . It typically is recommended for those with PD who have complications from medication such as dyskinesia and severe motor fluctuations, as well as those who no longer responding to pharmacological treatment 30 . The procedure can effectively reduce motor symptoms, which allows for a decrease in pharmacological medications 80 . The effectiveness can reduce L-dopa dosage, in turn reducing negative side effects that impact dietary intake, such as nausea, vomiting, and involuntary movements associated with the medication. Deep brain stimulation is also associated with an increase in appetite and restoration of hormonal balance. As a result, DBS promotes significant weight gain 52,76,81 . An investigation of weight gain in 30 PD patients receiving DBS found 29 participants (96.7%) experienced weight gain within one year of treatment 52 ; the mean weight gain was 9.3± 6.2 kg 52 . Just over 46% reported increased weight within the first three months 52 . Additionally, 24% of participants reported weighing the most in their lifetime 52 . None of the participants experienced weight loss and there was a clear shift from being underweight and normal body weight to being overweight and obese 52 .
Contradicting previous research, a higher prevalence of overweight and obesity in those with PD seems to exist compared to the general population 63 . Of 134 participants, 62% of participants were classified as obese or overweight, while 3% were classified as underweight 63 . The mean duration of PD was 10.6±5.3 years and mean age of participants was 65.9±8.9 years 63 . In comparing these participants to the general population, there was a higher proportion of obese people living with PD than living without PD (25 vs. 14%) 63 . However there seems to be an inverse relationship between the course of PD and BMI 63 . This highlights that while under-nutrition and excessive weight loss are an issue for those living with PD, weight gain and obesity are also present. Excessive weight gain and obesity are risk factors for CVD and other chronic diseases 82 Both weight loss and weight gain has been observed in this population and it is understood that nutritional status in those with PD is likely compromised 36 and to worsen as the disease progresses 1 . Consequently, a nutrition assessment, evaluation, 46 monitoring and possible treatments should be included in the treatment plan for those with PD 1 . Additionally, neurological disorders, such as TBI and stroke, with similar cognitive and physical complications as PD, may also experience malnutrition.

III. Traumatic Brain Injury
The Definition, Prevalence and the Effects of TBI. Traumatic brain injury occurs from an external mechanical force, such as a jolt or blow to the brain, that causes brain dysfunction 83 . There are two types of severe TBI's, closed and penetrating 84 . A closed TBI is caused by movement of the brain within the skull and can be caused by falls, motor vehicle accidents, or being struck with an object 84 . Penetrating head injuries are caused when a foreign object enters the skull and includes being struck with a sharp object or a firearm injury 84 .
Each year, approximately 1.7 million people in the US endure a TBI and about 275,000 are hospitalized 8 . In the US, the total annual economic cost of TBI is $60 billion 85 . Those sustaining a TBI is bimodal, occurring primarily in younger or older adults 86 . Older adults have the highest rates of TBI hospitalizations and deaths 8,87 . The leading cause of TBI is falls (35%), followed by motor vehicle-related injuries (17%) and a strike or blow to the head (workplace or sports-related injuries) (16.5%) 8 .
However, approximately 21% of the causes are unknown 8  Breed and colleagues 86 examined those who sustained a TBI up to four years ago, and noted that younger and older adults with TBI reported musculoskeletal issues more frequently than those living without TBI. In addition to physical impairment, acquired cognitive impairments as a result of TBI can impede everyday activities and interfere with productivity, independence as well as safety 91 . As a result, it is essential to manage the effects of TBI and analyze how cognition, nutritional status and physical function are impacted a year or more after injury.

TBI and Effects on Cognition
The cognitive effects following a TBI can last a life-time 86 . Neurological difficulties following TBI include seizures, spasticity, balance difficulties, loss of urinary control, communicative impairment, and chronic headaches 89 . Individuals who sustain brain injuries frequently have trouble with concentration, memory, perception, attention, social interaction, managing emotions, problem solving, and decision making 91 . These complications can interfere with multiple aspects of all aspects of daily activity 91 . A study analyzing functional status among OEF/OIF veterans with a history of TBI found reduced functional status was strongly correlated with poorer cognitive function 92 , particularly related to motor function, processing 48 speed and executive function 92 . These impairments highlight TBI's impacts cognitive functions related to carrying out ADL and to make decisions.
Cognitive complications in those living with TBI change over time. However, research indicates after a mild to severe TBI, cognition improvement occurs during the first two years, but remains impaired beyond this point 93 . During the early recovery phases, people seem to have problems with arousal, attention and memory 91 .
Although problems with attention and memory persist overtime, particular difficulties with executive function, attention and cognitive control mechanisms become more prominent 91 . A longitudinal study followed older adults with TBI for 12 months following injury, finding poor processing speed, verbal, memory, language and executive function compared to older adults without TBI 94 . Traumatic brain injury is also associated with increase risk for PD and other neurodegenerative diseases 95,96 .
Furthermore, older adults with closed TBI tend to have issues with naming and word fluency under timed conditions, as well as with verbal and visual memory 97 .
Impaired cognitive function in this population seems to exacerbate other health related issues 3 and the Brain Injury Association of American recognizes additional research is necessary to further understand the disease and develop clinical guidelines and modifications 91 . Additionally, how these cognitive issues impact dietary intake, nutritional status and whether they promote nutritional risk needs to be further examined.

Physiological Side Effects and Energy Needs of TBI
Research has extensively examined the physiological side effects and impact on nutritional status during the acute phase of TBI, from time of diagnosis to six 49 months 10,11 . The body undergoes hyper-metabolic, hyper-catabolic, and hyperdynamic responses 13 . These physiological responses are not only a result of the injury, but due to unfavorable secondary events from TBI 98 . These secondary events include fever, increased intracranial pressure, and seizures 98 Consequently, following a TBI the body's energy expenditure and nitrogen excretion increase 14 . This increased energy expenditure results in a catabolic state, increasing muscle breakdown as well as negative effects on immune function and morbidity 99 . Energy and protein needs increase and meeting these requirements is imperative to prevent and prolong muscle wasting and excessive weight loss 13 . To treat those with a TBI during the acute phase, early nutrition support decreases risk for morbidity and mortality 100,101 .
A retrospective study explored nutritional treatment (parenteral and enteral nutrition) and outcomes up to six months after a TBI 13 . A nutrition assessment found 68% participants exhibited signs of malnutrition during this time period, with up to 29% body weight loss 13 . This study revealed that in most participants weight continued to decrease one to two months after injury 13 , highlighting the increase in energy expenditure and importance of adequate nutrition during the immediate stages.
However, what happens beyond this point in those living with a TBI needs to be further examined.

Malnutrition and TBI: Under-nutrition
Nutritional status following the acute phase of a TBI has not been extensively examined. Research has been reported immediately following a TBI and found those living with TBI seem to reach lowest weight two months after injury 13 . Research has 50 also examined nutritional status up to six months after injury, typically this time is the rehabilitation stage 13 .
While research has not examined nutritional status in those living with TBI a year or more, chronic complications following a TBI may compromise dietary intake and lead to poor nutritional status 3 . Self-reported chronic issues of TBI include changes in weight and appetite, sensory changes, swallowing problems, chronic pain and dystonia (a neurological movement disorder) 3 . Due to similar chronic symptoms in those living with PD and TBI, there is reason to assesses the impact physical and cognitive disabilities, including depression associated with TBI 3 , has on nutritional status and ability to buy and prepare food. This is especially true since research has shown physical and cognitive disabilities impact dietary intake and promote difficulty preparing meals in those living with PD 1,36,68,69,70 .
In a systematic review, Murphy and Carmine 3 note dysphagia is common immediately following a TBI, and can persist or even worsen overtime. Achieving adequate nutrition and hydration can be a lifelong challenge for those living with TBI and dysphagia 3 . Compared to the general population, those with TBI are two and a half times more likely to die of digestive disorders 102 . The most common digestive disorders include gastro-esophageal reflux disease, which occurs when acid re-enters the esophagus due to irregular relaxation of the lower esophageal sphincter. It can cause heartburn, regurgitation, dysphagia, aspiration pneumonia, chest pain and nausea 3 . While, gastrointestinal disorders can cause a decrease in dietary intake and weight loss, it is often caused by obesity, use of steroid medication and hiatal hernia 3 .

Malnutrition & TBI: Over-nutrition
A common late-onset complication of TBI is weight gain 3 . Excessive weight gain associated with TBI can be due TBI's impact on metabolism and hormone production, memory, self-regulation, mobility, altered satiety cues, and appetite altering medications 3,86 . Weight gain for those with disabilities significantly increases risk for CVD, diabetes, functional dependence, and immobility 3 . Weight gain in TBI is associated with metabolic syndrome, which can lead to stroke, retinopathy, peripheral artery disease, diabetes and cardiovascular disease 3,86 .
Additionally, TBI is associated with post-traumatic hypopituitarism (PTHP) (decrease in the release of pituitary hormones to regulate homeostasis in the body); approximately 25% of long-term survivors have post-traumatic hypopituitarism 103 .
The number of people with PTHP after a TBI is a concerned because the condition is associated with increase in weight and metabolic imbalances up to two months after a TBI 104 . The pituitary gland is a vital link between the nervous system and endocrine system and releases hormones that impact metabolism and other life processes 105 . It is often undiagnosed in those with TBI because of the underlying primary diagnosis of TBI, but can be treated with hormone replacement therapy 103 . Klose and colleagues 23 found those with TBI and PTHP have higher body compositions and BMI compared to those without PTHP up to 12 months after injury. An increase in BMI from three months (27.1 ± 5.7 kg/m 2) after injury to 12 months (29.3± 5.7 kg/m 2 ) was found 23 .
Those with PTHP were also older, and had a more severe TBI. What happens beyond this point regarding weight and body composition needs to be examined.

52
Weight change is a common theme in those living with TBI 23 . Hibbard and colleagues 89 found those living with TBI for a year or more reported unintentional weight loss or gain greater than ten pounds. However, to our knowledge, the research has not examined long-term (12 or more months following TBI) weight status and dietary intake in people with TBI. How diet, as well as physical inactivity, plays a role in weight gain and if weight gain continues overtime needs to be examined. Since research indicates nutritional status and weight change occurs in TBI, a form of ABI, it is likely that changes also occur in those living with other forms of ABI, such as stroke.

The Definition, Prevalence and Effects of Stroke
A stroke results when the brain's blood supply is blocked or when a blood vessel in the brain bursts 106 . The American Heart Association (AHA) estimates that someone in the US has a stroke every 40 seconds 82 . By 2030, nearly 4% of the US is projected to have experienced a stroke, and there will be an additional 3.4 million people with stroke compared to in 2012 107 . Stroke is the fourth leading cause of death 106 and 80% of stroke can be prevented 106 . Maintaining a healthy diet and exercising are to ways to help prevent a stroke 108 . Eating five servings of fruits and vegetables per day has been found to lower risk of stroke by 30% 108 . Additionally, a meta-analysis found those who had high physical activity levels had a 27% lower risk of stroke 109 . Stroke occurs mostly in adults over the age of 65 7 . Women ages 55-75 have a one in five chance of stroke, while male counterparts have a one in six chance 110 ; each year approximately 55,000 more women than men have a stroke 111 .

53
Although age-specific stroke rates are high in men, women have much higher incidences at older ages due to the longer life expectancy in women 112 .
The total annual direct and indirect costs of stroke are forecasted to increase to $240.67 billion by 2030, an increase of 129% 107 . Immediately following a stroke, at least 40% of stroke survivors have moderate disabilities and up to 30% have severe disabilities 113 . A stroke may impact psychological, physical, social and cognitive function 114 . These complications can alter a person's life and increase risk of being institutionalized, becoming psychotic or depressed, or of dying 114 . Of a 180 people over 65 years old, six months after stroke, 50% had hemiparesis, 46% had altered cognitive function, 35% had symptoms of depression, 30% were unable to walk without assistance, and 19% had aphasia 19 . Similar to PD and TBI, side effects of stroke impact physical and cognitive function and may also lead to assistance with ADL 115 , as well as a decrease in dietary intake and quality overtime.

Stroke and Effects on Cognition
Cognitive-linguistic deficits following a stroke reduces functional outcome for at least five years after stroke in some individuals 116 . Assessments of cognitivelinguistic function after stroke assess memory, information processing speed, visuoperceptual/construction ability, EF, attention, language and depression 114,117 . Impaired memory, poor concentration and mental slowness are the most common cognitive complaints after a stroke 118,119 . The functional status of 126 stroke patients was examined, (mean age 76.9 ± 10 years) at baseline (2-3 weeks after stroke) and 13 months following event of stroke 120 . Findings concluded cognitive function at baseline 54 was an independent and significant predictor of long-term functional outcome and degree of disability after stroke 120 .
Subjective cognitive complaints in 25 older adult stroke patients (mean age 67±10 years) were assessed three to nine months after stroke and revealed 90% of participants reported cognitive issues or impairment 4 . Another study found attention, language, construction and reasoning the most affected cognitive limitations, where orientation was least affected 121 . Depression was the main variable that made a significant independent contribution to the prediction of subjective cognitive complaint 4 . In general, cognitive decline, is associated with risk for functional decline in ADL 122 , which can impact dietary intake and physical activity level. Whether these cognitive issues in junction with physiological side effects of stroke impact dietary intake and physically activity level, as well as increases risk of reoccurring stroke must be assessed.

Physiological Side Effects and Energy Needs of Stroke
Similar to TBI, the physiological side effects and impact of nutritional status during the acute phase of stroke has been thoroughly examined 15,123 . Following a stroke the body is in a hyper-catabolic state, which increases energy needs 15,16 . These energy needs are usually not met and as a result, fat and muscle tissue wasting and weight loss occurs ( Figure B) 15 . The body's response to stroke leads to functional decline and the depletion of energy stores 15 . People who experience tissue wasting may also experience cachexia (dramatic weight loss and muscle wasting) 124 or sarcopenia, which can contribute to a poorer prognosis after stroke 15 . 55 Figure B: 15

Malnutrition and Stroke: Under-Nutrition
In addition to weight loss from this hyper-metabolic state, persons in the acute phase of stroke are susceptible to weight loss due to fever, local central nervous system damage, and cytokines and oxygen-free radical build-up due damage of the blood vessel lining 15 . Impaired feeding and dysregulation of appetite can also promote weight loss following a stroke 15 . Finally, inactivity due to paralysis, can promote weight loss due to a loss of lean muscle mass 15,125 , and severely interfere with one's ability to prepare meals. As a result, malnutrition can result from inadequate intake of kilocalories, protein and/or nutrients the body requires for maintenance and repair 115 .
Malnutrition as a result of stroke can negatively impact physical and social well-being and quality of life 126 .
Decline in nutritional status during the acute phase of stroke is highlighted in a prospective, descriptive study examining the risk and prevalence of malnutrition of 23 participants 123 . At baseline, 21 of 23 participants were considered well-nourished, however significantly more participants were malnourished or at risk of becoming malnourished ten days later 123 . Based on MNA scores, after ten days, eight participants (35%) were well-nourished, nine (39%) were at risk of malnutrition and six (26%) were malnourished 123 . The MNA not only exams anthropometrics, but also includes a dietary questionnaire, as well as a global and subjective assessment. While MNA scores indicated decline in nutritional status, there was no significant change in weight and BMI scores between these two time periods 123 . Despite a small sample size, this decline in nutritional status highlights rapid changes that occur during the acute phase of stroke. Impaired feeding during the acute phases of stroke can be due dysphagia, and up to 65% of people with stroke experience dysphagia 126 . Many regain functional swallowing usually within the first month following a stroke 127 , however, for some, dysphagia is still present six months after stroke 128 . Dysphagia can compromise food and fluid intake, which can alter consciousness and promote physical weakness. The physical weakness experienced post-stroke can also negatively impact swallowing.
Complications from dysphagia can also increase length of hospital stay, rehabilitation time, and result in a poorer long-term outcome 126 .
Change in consciousness, difficulty swallowing, inadequate food and fluid intake, and an increased in energy expenditure as a result of stroke can result in severe malnutrition 15,126 . Whether nutritional status improves or further declines after the acute phase needs to be more closely examined. Since nutritional status is likely to decline in the acute stage, where there is closer monitoring over dietary intake, it is necessary to examine what happens to nutritional status in people with stroke as time progresses.
Westergren 5 found stroke survivors who self-reported low energy levels, were more prone to poor nutritional status, since they may stop eating before daily energy needs are meet. Research has examined nutritional status in the month following a stroke, and found chronic disabilities that interfere with ADL related to eating including purchasing groceries, preparing food, and eating 5 . Eating difficulties, barriers that negatively interfere with the preparation and intake of food and fluids 129 , are common among stroke survivors and negatively impact dietary intake, as well as quality of life 123,130 . Eating difficulties (sitting position, managing food on plate, transporting food to mouth, opening and closing mouth, manipulating food in mouth, swallowing, food consumption, alertness and eating speed) related to stroke were observed.
A comparison of eating difficulties and nutritional status in the acute phase (the days immediately following stroke) was compared with nutritional status three months after stroke. The research found that majority of baseline eating difficulties, observed continued three months later. Inadequate food intake, increased in 22 participants in the acute phase to 32 participants post intervention 17 . Despite these observations, nutritional status, based on total MNA scores, significantly improved three months after a stroke 17 . The contradiction of improved MNA scores compared to the observed inadequate food intakes, suggests nutritional status in those with stroke needs to be examined more thoroughly, and that the MNA may not be an effective tool in assessing nutritional status overtime in this population.
Other research has highlighted malnutrition to be an issue beyond the rehabilitation phase and up to six months after stroke compared to the acute 58 phase 131,132 . Six months after stroke 82% of women and 78% of men with eating disabilities did not meet energy requirements. Nutritional status, male gender, age, and stroke severity at admission were significant risk factors for poorer functional outcomes six months post-stroke 16 . Weight loss as little as three kilograms or more following a stroke has been an independent predictor of adverse outcomes following stroke 133 , this weight loss has been found to occur up to a year 134 . As a result, malnutrition during acute stroke is considered a potentially modifiable factor that should be corrected and monitored to help improve long-term functional 16 . Whether weight loss continues to persist after a year following stroke must also be assessed, especially since many eating difficulties are associated with stroke 135 ..
Eating difficulties following a stroke highlights that individualized therapy after stroke to improve eating ability is imperative 135 . More research is needed to understand whether malnutrition persists a year or more after stroke, as well as preventing stroke reoccurrence. Additionally, due to the susceptibility of malnutrition in the months following a stroke, an obesity paradox exists. While, being overweight/obese increases risk of stroke, 22% and 64% respectively 136 , research has found an obesity paradox following a stroke 137 . Being overweight or obese at the time of stroke seems to result in better long-term functional outcomes for those living with stroke 137 .

Malnutrition and Stroke: Over-nutrition
An obesity paradox seems to exist with stroke patients, in that mortality seems to be lower in obese patients 137 . Those who are underweight at the time of stroke seem to have more complications and poorer survival than those who are of normal 59 weight or overweight when assessed six months after stroke 138 . The underlying cause of this paradox is currently unknown, but supported from research with large study populations 139 . The notion of the obesity paradox and stroke is often attributed to the catabolic imbalances and inflammatory state immediately following a stroke that causes weight loss 15 . This weight loss also causes muscle tissue wasting, which impairs recovery after stroke 15 .
While obesity increases risk of a first-time stroke, however, those who are overweight or obese post-stroke, are less likely to have a reoccurring stroke in the years following stroke 139,140 . Through examining data form the Danish Stroke Registry, Andersen and Olsen 140 found as BMI increases, the risk of a stroke reoccurring decreased, despite age, sex, stroke severity or cardiovascular risk profile.
Underweight patients more likely had a history of a previous stroke 140 . However, other research indicates, normal weight patients were more likely to have a reoccurring stroke 24 . This is a concern since research implicates compromised dietary intake in six months following 129 , which can promote a further decline in weight.
The obesity paradox seems to persist as time following a stroke progresses. A prospective study examined stroke survivors up to 30 months after stroke or a transient ischemic attack, and found overweight and obese participants to be at the lowest rink for the following endpoints: morbidity, mortality, and poor functional outcomes 24 .
Those positive outcome measures were found the most in obese or very obese, while underweight participants were at the highest risk for all endpoints 24 .
Overall, existing research supports obesity paradox and stroke, however a recent study examining stroke rehabilitation outcomes, slightly contradicts the idea of 60 obesity paradox 141 . The relationship between functional independence measurement (FIM) scores, including cognitive and motor sub-scores, and BMI scores for those in stroke rehabilitation was examined and those considered overweight had the highest motor and cognitive sub-scores 141 . There was no significance differences between motor FIM sub-scores between groups, but the overweight group had significantly higher cognitive sub-scores compared to the obese group 141 . No significant differences were found between normal weight stroke participants and underweight or overweight participants for cognitive sub-scores 141 . Whether this holds true beyond the rehabilitation phase has not been assessed, and highlights the need to develop proper guidelines for weight status and dietary intake following a stroke. Especially since research has found an association between obesity and poor cognition in the aging population 142 .
Due to mixed results, more research is needed understand how to help optimize health and prevent a reoccurring stroke or other forms of chronic disease. Research regarding the obesity paradox and stroke contradicts current guidelines to reduce body weight after stroke 15 , and clearer guidelines are needed to promote optimal weight status in this population, especially long-term (a year or more) after stroke. Stroke is a cardiovascular event, and as a result it is important to continue to assess the cardiovascular risk of this population to prevent the occurrence of another cardiovascular event. Due to the similarities this neurological condition has with TBI and PD, the cardiovascular health of these populations must also be examined.

V. Overall Cardiovascular Risk
Across these three disease states research varies as to whether or not those living with neurological conditions such as PD, TBI and stroke are at increased CVD risk 3,52,63,143 and this may be due to change in lifestyle following diagnosis as well as physiological impacts of the disease. Cardiovascular disease is the leading cause of death in the United States 144 . It is the disease of the heart and/or blood vessels and often results from atherosclerosis, which is the hardening of the arteries 145 . Modifiable CVD risk factors include being overweight or obese, having hypertension, elevated blood glucose levels, and dyslipidemia 146 . As well as life style choices such as physical inactivity, tobacco use and a diet high in saturated fat and processed foods and low in fruits, vegetables and fiber 146,147 .
To assess if one is overweight or obese, BMI and %BF are indicators.
Body mass index is calculated from weight and height and can serve as an indicator of body fatness 148 . Body mass index is classified according to predetermined categories: underweight = <18.5 kg/m 2 , normal weight = 18.5-24.9 kg/m 2 , overweight = 25-29.9 kg/m 2 and obese ≥ 30 kg/m 2 148 . According to the American Council on Exercise 149 , any female with ≥32% BF and any male with ≥25% BF are considered obese.
Blood pressure is a clinical risk factor for CVD. Systolic blood pressure (SBP) >120 mmHg and diastolic blood pressure (DBP) >80 mmHg are considered suboptimal. When diagnosing for metabolic syndrome, SBP >135mmHg and DBP >85 mmHg are used; these levels are considered pre-hypertensive 150 . Hypertension can be caused by lifestyle factors such as a high sodium diet, obesity and physical inactivity 151 . Suboptimal serum levels are also a risk factor for cardiovascular disease and can be affected by poor diet and physical activity 152 . Total serum cholesterol >200 mg/dL, low density lipoprotein cholesterol (LDL-C) >100 mg/dL, high-density lipoprotein cholesterol (HDL-C) < 40 mg/dL, and triglycerides > 150 mg/dL are used to describe those with dyslipidemia 153 . Dyslipidemia can lead hardening of the arteries overtime, which can lead to CVD 154 . Hyperglycemia is marked by fasting blood sugar > 100 mg/dL 150 and can indicate insulin resistance, metabolic syndrome, pre--diabetes (110-125 mg/dL) or diabetes (>126 mg/dL) 155 .
The development of clinical and biochemical CVD risk factors are impacted by diet and physical activity. An inverse relationship has been found with fruit and vegetable consumption and the risk of CVD 147 . Consuming fruits and vegetables >3 times a day compared to once a day was associated with a 27% lower stroke incidence, a 42% lower stroke mortality, and a 27% lower cardiovascular disease mortality 147 . Increasing fiber intake, which can be found in fruits and vegetables and whole grain products, has also been found to reduce modifiable CVD risk factors such as dyslipidemia, diabetes and being overweight [156][157][158][159] . Physical inactivity can also negatively impact blood pressure, lipid profiles, fasting blood glucose and weight, which in turn can lead to a cardiovascular event 160 .
In addition to modifiable risk factors that can increase risk of CVD, Nonmodifiable CVD risk factors include age, gender, race and family history 145 . Risk of developing heart disease increases with aging 145 . Men are at greater risk of heart disease than pre-menopausal women, however once women are post-menopausal risk is similar across both genders 145 . African Americans seem to be at greater risk for developing CVD 161 . Finally, risk also increases if a first-degree relative had a cardiovascular event before the age of 55 145 . To assess and treat these risk factors, the 63 American Heart Association and American College of Cardiology developed 10-year and lifetime risk estimates using algorithms for the development of atherosclerotic cardiovascular disease (Figure C) 162 . As described previously, those living with PD, TBI or stroke experience changes in physical and cognitive function 3 , which can not only impact nutritional status and dietary, but also promote a sedentary lifestyle, which may increase the risk of CVD in this population.
Research indicates those living with neurological conditions such as PD, TBI and stroke may be at increased CVD risk because they have one or more of these modifiable risk factors, such as a sedentary lifestyle, elevated lipid profiles or inadequate diets 3,52,63,143 . As described earlier, neurological conditions can impact dietary intake, especially for those living alone. Generally, older men living alone are at risk of malnutrition and need a supportive environment to provide optimal dietary intake and help compromise cardiovascular health 163 . A recent study analyzed the daily eating events among older men living with PD, stroke or rheumatoid arthritis and found that men living alone used more convenience foods such as instant and readyto-eat foods, compared to those who lived with a significant other 163 . Convenient foods are often higher in sodium, sugar and fat compared to fresh, homemade meals and can increase risk for chronic disease, including CVD 164 . A late-onset complication of TBI is weight gain which can be a result from hormone and metabolic imbalances, as well as changes in mobility, self-regulation, altered satiety cues, and from medications that alter appetite 3,86 . Weight gain can lead to metabolic syndrome, which seems to develop in many of those living with TBI 3 .
Metabolic syndrome is associated with excess food consumption, which can greatly be due to larger portion sizes, convenience foods and the availability of foods high in 1 Algorithm developed by The American Heart Association and American College of Cardiology to estimate 10-year and lifetime risks for the development of atherosclerotic cardiovascular disease (ASCVD) saturated and trans fats and added sugars 165,166 . The prevalence of metabolic syndrome can also increase risk for the development of CVD in this population 3 . Yet, the prevalence of those with TBI who have CVD or may be at risk for CVD has yet to be assessed.
Meanwhile, the prevalence of overweight and obesity seems to change throughout the course of PD, depending on the stage of PD and side effects of medications 1 . Research has found a lower prevalence rate of stroke in those with PD compared to the general population 167 . The mechanism behind this is not fully understood. There seems to be a higher prevalence of those overweight and obese with PD compared to the general population, however being overweight/obese with PD does not seem to increase risk for CVD 168 . While, research has found this association, the mechanism is still not quit understood, and as result monitoring weight is necessary to help prevent other declines associated with excessive weight gain.
Besides weight, research has also analyzed lipid profiles in those with PD. The relationship between cardio-metabolic risk factors and duration of PD has been examined to find that the longer one is living with PD, the better HDL-C levels are 22 .
An inverse relationship of the TC-to-HDL-C ratio was also observed 22 . Research has also examined the effect of lipid profiles on those with TBI. Hypopituitarism is a common side effect following TBI and those living with TBI and PTHP frequently present metabolic alterations that include altered glucose levels, insulin resistance and hypertriglyceridemia and dyslipidemia 169 .
In a total risk assessment, patients with a TBI appear to be at significantly increased risk for stroke 170 , as well as diabetes mellitus, hypertension, atrial fibrillation and CVD 3,16,89,[170][171][172]  When enough cardiovascular risk factors are present, this can lead to a cardiovascular event. Traumatic brain injury is associated with increased risk of stroke, a population based study followed those living with TBI for 5 years after injury, and found TBI patients had 10.21 times, 4.61 times and 2.32 times greater risk of stroke compared to non-TBI patients at 3 months, one year and five years post diagnosis 170 . At three months following TBI diagnosis, 675 strokes occurred in those with TBI, while only 207 cases were reported in non-TBI patients 170 . This study speculates the increase risk of stroke in those with TBI can be from the disturbance of blood supply to the brain post TBI, the formation of an atherosclerotic blood vessel due to the sudden impact after a TBI, or an increase in intracranial pressure and blood pressure post TBI 170 . Antipsychotic drugs used to treat TBI may also increase risk of stroke 173 . The presence of cardiovascular risk factors previously described in this population 3,23 , as well as the role diet and physical inactivity plays in developing CVD risk factors may also increase risk of stroke. As a result a more thorough assessment to understand the relationship between TBI and a stroke event is warranted. Additionally, since both TBI and stroke are forms of ABI, the presence of CVD risk factors in TBI give warrant an examination of CVD risk n those living with stroke.
Whether those living with stroke remain at cardiovascular risk following event of stroke needs to be assessed. As described earlier, an obesity paradox seems to exist following stroke, and is associated with a decrease risk in stroke reoccurrence 143 . The AHA proposed guidelines to prevent stroke reoccurrence, target similar modifiable and non-modifiable risk factors associated with CVD prevention 174 . The guidelines note that while obesity increases risk of stroke, no study has found weight reduction to reduce risk of stroke recurrence 174 . Additionally, Andersen and Olsen 140 found patients with recurrent stroke are more often men, underweight and have a history of heart attack, atrial fibrillation, and hypertension. This study highlights the negative correlation between BMI and stroke recurrence based on an odds ratio (OR) ( Figure   D) 140 . It also highlights that risk factors for stroke and other cardiovascular events continue to exist in those following stroke if lifestyle modifications are not made.
A final modifiable risk factor that increases the chances of developing CVD is smoking tobacco. Smoking increases risk for coronary heart disease and stroke by two to four times 175 ; it can also reduce blood flow to legs and skin 175 . The prevalence 68 of smoking amongst those with neurological diseases and the influence it has on cardiovascular health in this population needs to thoroughly be examined. In addition to lifestyle choices, such as smoking tobacco, physical activity and function are associated with cardiovascular risk. Due to the nature of these three diseases, physical activity level may be limited. Physical impairment can promote a sedentary lifestyle and weight gain, but also negatively impact lean body mass.

VI. Physical Activity and Physical Function
Physical activity is bodily movement by the skeletal muscles that results in energy expenditure 176 . It includes leisure time activities, such as sports and exercise, and ADL 176 . Physical activity curtails risk of mortality and morbidity 160 . Health benefits of physical activity have been well documented, including weight management, and preventing and treating cardiovascular disease and musculoskeletal 69 disorders 160 . Physical activity promotes good physical health status, as well as mood and cognitive function, which can improve quality of life 177 . Evidence shows physical activity can help reduce age-related physical and cognitive decline [178][179][180] . A recent study examined the impact of a physical and leisure activity programmed on community-dwelling older adults and found the intervention had improvement in areas of cognition, specifically in abstract reasoning ability, a common initial symptom of dementia 181 , as well as significant in QOL.
Physical activity greatly relates to physical function, which is one's ability to carry out tasks related to activities of daily living, as well as quality of life 182 . Limited physical function can be due compromised upper and lower extremity function 122 .
Compromised physical function can interfere with performing different tasks such as walking, climbing stairs, lifting heavy objects, picking up an object off the floor 183 , bathing, dressing, eating and cleaning 184 . A decline in physical function may lead to sedentary behaviors, which combined with excess calorie intake, can increase risk for obesity 185 . Obesity is further associated with functional limitations 186 .
Many older adults develop sarcopenic-obesity, and this increase in body fat and decrease in muscle mass has been found to accelerate decline in physical function 183,187 . To treat and prevent complications of sarcopenic-obesity, incorporating physical activity can increase muscle mass and decrease fat mass, and in turn enhance physical function 188 . However, low BMI scores are also associated with compromised physical function, resulting in increased risk of falls and inability to carry out ADL 189 .
Guidelines for physical activity have been created to promote optimal health benefits 190  Despite these health benefits, some adults living with disability may not be able to meet these guidelines due to cognitive and physical impairment. For those living with disability, any degree of activity can provide health benefits and curtail functional decline 193 . Physicians can modify physical activity recommendations for those unable to meet guidelines 193 , but realities of these neurological disorders must be recognized to help this population overcome barriers of the disease that may deter participation in physical activity.
Physical and cognitive disabilities associated with neurological diseases can greatly impact physical function, which may decrease physical activity level and can also result in a decline in quality of life and depression 3,4,39,194 . A decline in physical activity is a risk factor for decline in physical function and can further inhibit mobility 122 . Consequently, those living with PD, TBI or stroke are at risk for sedentary behaviors and further induced functional decline, especially since these diseases can greatly impact movement of arms and legs 185 .
Motor and non-motor motor symptoms associated with PD may impact physical activity and function. . A reduction in physical function can also reduce ADL such as housekeeping, preparing meals, and ability to travel in the community 195 .
Additionally, Wild and colleague's 27 dual task study, revealed people with PD had a shorter gait due to difficulty with performing a cognitive task in conjunction with a motor task. Additionally, those with PD that had postural instability and gait difficulty reported worse health-related quality 38 . Changes highlight the impact both motor and non-motor symptoms have on PD, resulting in life-style changes.
Physical and cognitive changes experienced in this population may also increase risk for falling. Falls not only impact well-being, but can result in severe injuries 196 . Factors that increase risk for falls include older age, body composition, number of chronic diseases, muscle strength, functional mobility, balance, and fear of falling [197][198][199] . Targeting these risk factors by promoting physical activity that targets muscle strength and balance may help to prevent falls in this population, as well as those with other neurological disorders.
Extensive research indicates those with PD and stroke are at increased risk for falls 200,201 . Approximately 60% of those living with PD fall yearly 202 . Predicting falls in those with PD are associated with history of previous falls, disease severity, poor balance, reduced mobility, freezing of gait and reduced leg strength 203,204 . Similar physical limitation following a stroke also increase risk of falling 205 , and it is one of the most common complications following a stroke 206 .
Following a stroke, impaired dynamic balance is associated with frequent falls three weeks after stroke 205 . Those who experience falling after a stroke show lower cognitive and physical functions, compared to those who did not fall, which highlights falling may impact cognitive and physical function 205 . This loss of balance, combined with fear of falling, may promote a sedentary lifestyle and decline in physical activity level.
Additionally, immediately following a stroke, walking dysfunction is common, as well as fatigue and lack of energy 5 . To treat these symptoms rehabilitation is usually followed after a stroke. Research also reveals rehabilitation post stroke is a key time to assess cognitive function, and that stroke-related cognitive impairment can limit functional gains during stroke rehabilitation 200 . Also, despite rehabilitation physical limitations can persist or re-occur 20,130 . Six months following a stroke, among 206 participants, 75% experience upper limb/motor impairment 130 . Research has also found three to nine months following a year-long rehabilitation, those living with chronic stroke seem likely to redevelop symptoms of walking dysfunction [207][208][209] .
Additionally, research has found gait seems to worsen in the later years post stroke 20 , which can present challenges with balance, an increase in energy expenditure, risk of injury and decrease activity levels 20 . These findings insinuate rehabilitation exercises beyond the rehabilitation phase may be necessary to promote and maintain optimal physical function in those living with chronic stroke.
The literature also implies those living with TBI may be at increase risk for falling 3,7 . This can be due to changes in strength, endurance and balance 210 , as well as diminished motor-planning and attention, pain and weight gain 3 . All of these factors are inter-related and can promote poor physical function and low physical activity levels. While a decline in mobility is a part of the natural aging process, it seems to happen more rapidly in those living with TBI 3 .
Those who sustain a TBI are also more likely to experience muscular and orthopedic symptoms compared to nondisabled people 86 . Change in mobility, pelvis, limb and vertebrae fractures and other physical traumas that occur at the time of injury can also have long-term consequence and can re-emerge overtime, thus decreasing physical function and activity level and promoting weight gain 3 . Pain and stiffness in the joints may also deter physical activity in this population 3 . If this population continues to be sedentary and obesity develops, pain can become more pronounced, as research has found an association between obesity and joint and muscle pain 211 . Since over-nutrition has also been found in those with PD and stroke these issues may also occur in these neurological disorders as well.
As previously described, those with PD, TBI or stroke can suffer from underand over-nutrition. As a result, both physical inactivity and being obese are associated with decline in physical function and associated risk factors, such as the development of metabolic syndrome, CVD, and diabetes 193 . Being underweight can result in muscle wasting and poor physical function 18 . As previously described those with disability that are underweight may have issues with eating and swallowing which can also promote decline in physical function 129 .
Issues of physical function are prevalent in all three of these disease states and can further negatively impact health and quality of life. While, functional decline is a natural part of aging, it is more severe for those living with neurological conditions 74 and other chronic diseases 193 . A recent cohort study examined factors associated with changes in physical function in older Chinese adults and found the main cause of functional decline was chronic disease; older persons with chronic conditions, such as stroke, PD, diabetes, and osteoporosis were more likely to experience a decline in physical function over the four year study period 193 . This study highlights that while chronic diseases increase the likelihood of disability, information regarding effective management of these disabling conditions is limited 193,212 . Research has also yet to examine the role of combining nutrition, cognition and physical activity in this population and how it can positively improve health outcomes.
Cognitive decline associated with these disease states can also impact physical activity level and physical functioning. Even mild levels of cognitive impairment have been found to increase disability and overall functional impairment 10 . Those with cognitive impairment may not be able to effectively perform meaningful tasks, which is hypothesized to be closely linked to inability to carry out ADL 213 . Besides poor cognition, psychological issues associated with these neurological disorders, including fear of falling is recognized as a factor that may deter older adults susceptible to falls from being physically active 198 .
While existing barriers can lead deter physical activity and promote decline in physical functioning, certain factors in this population have been found to help curtail this decline. A recent study examining factors that impact exercise behavior of 260 participants living with PD contradicts this 214 . The study found that those who participated in exercise had less severe motor impairment, fewer depressive symptoms, and few issues with physical mobility. Through a multivariate logistic 75 regression, this cross sectional study found the degree of physical impairments, activity limitation and participation restrictions were not significantly associated with exercise behavior, but self-efficacy and belief regarding capabilities to exercise were 214 .
Regardless of disease severity, those with higher self-efficacy were more than twice as likely to participate in routine exercise compared to those with low selfefficacy 214 . A higher education level and older age also was associated with increased likelihood to partake in exercise 214 . The majority of participants (86%) had mobility related issues that disabled them from participating ADL, but 88.8% of participants had a social support system at home to assist them 214 . This highlights that the main source of physical activity for this population is from planned exercise and leisure activity, as opposed through independently carrying out ADL. Findings also imply that promoting an increase activity in this population may be most effective through encouraging exercise and leisure time activity.
A limitation of this study was that the majority of participants only had mildto-moderate PD. Additionally, due to the cross-sectional study design, causality as to whether exercise promotes high self-efficacy or high self-efficacy promotes exercise needs to be monitored overtime 214 . How the progression of the disease impacts selfefficacy, willingness to exercise overtime, and whether exercise overtime can help delay the progression of the disease must also be assessed 214 .
Never the less, the findings of Ellis and colleagues 214 215 . The long-term disabilities of these neurological diseases greatly impact QOL 3,4,58 . Quality of life has been shown to be lower in those with PD compared to age-matched healthy controls as well as compared to those with other disease entities such as diabetes 216 . A recent study, examined resilience, or one's ability to "bounce back" following an event or diagnosis, in those with PD. Results found that those with higher resilience scores, had better physical and mental quality of life and lesser disability 217 . However, no correlation was found between disease severity and resilience scores 217 . Depression and mild cognitive impairment in those with PD is also correlated with a poorer nutritional status, indicating a worse QOL 1,36,68,69 . Those living with TBI and stroke also experience mental and physical side effects, which can also experience changes in QOL 72 .
Those with TBI often experience side-effects that compromise well-being, such a bowel and bladder incontinence, sleep disorders, psychiatric diseases and sexual dysfunction 218 . Additionally, Siponkoski and colleagues 219 examined the quality of life of those with TBI that received intensive multidisciplinary residential rehabilitation treatment for up to 15 years post injury, and found quality of life was related to age at time of injury, depression, anxiety, amount of assistance needed, and education level 219 . Results also found that QOL remained stable over time and that those with milder injuries had a lower QOL 219 . Traumatic brain injuries can impact long-term functional outcomes in older adults, however more information is needed to identify the specific, long-term post TBI side effects have on ADL, especially in older adults 28 . Jacobsson and Lexell 220 examined life satisfaction in those living with TBI six to fifteen years after injury and found those with a higher life satisfaction had fewer emotional disturbances and better social participation, as well as a longer time post injury and a more severe injury sustained later in life. It appears cohabiting and higher productivity levels also helps improve life satisfaction 220 . Findings indicate life satisfaction can improve with time and highlight factors that can impact life satisfaction. Both studies indicate more severe cognitive impairment seems to be associated with greater QOL and life satisfaction 219,220 . The reasoning for this, as well as the impact disease severity has on other health parameters, needs to be further investigated.
Quality of life is also impacted in those with stroke, which can be exhibited by eating difficulties and inability to perform activities of daily living 5 . Research also consistently finds women seem to have less favorable outcomes after stroke than men, more difficulty with ADL, depression and overall lower QOL 112 . This lower QOL in women could be due to worse mobility, pain/discomfort, and anxiety and depression observed up to 12 months after stroke 221  Disorder's LOUD Crowd and Gateway Wellness Café. Study staff explained the research project to potential participants. If a potential participant was eligible and interested, they signed two copies of an informed consent. This sub-study only included baseline assessments, but participants consented to participate in a five-year longitudinal study with assessments every six months. Participants were then assigned identification numbers for data management that did not include any identifying numbers or letters.
The study utilized baseline data collected from November and December 2013.
Written data was stored in a locked file cabinet in 203 Fernwood on the URI campus.
Electronic data with identified information was stored on a computer in 203 Fernwood and password protected and encrypted. De-identified data sets (identifying information like name address, email and telephone numbers removed) were stored on passwordprotected computers in Ranger 301 (Lofgren's lab) and 214 Independence Square (Delmonico's lab).

Protocol Overview
Participants reported to a URI Speech and Hearing Clinic location for baseline assessments. Baseline assessments were conducted on two separate occasions. After signing informed consent, participants completed cognitive, nutrition, and physical function assessments. Participants fasted 12-hours prior to the assessment, but were encouraged to drink water during this fast. During the assessment, a 12-hour fasting blood sample was collected, as well as blood pressure. Nutritional status was examined using assessment tools that reflect dietary quality, anthropometrics, body composition and biochemical values.
All questionnaires were administered to participants by study staff. The following surveys related to cognitive-linguistic capacity, nutrition and physical functioning and physical activity were completed: The Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) 1 , the Swallowing Quality of Life Survey (SWAL-QOL) 2,3 , the Dietary Screening Tool (DST) 4,5 , and Physical Activity and Disability Survey (PADS) 6,7 . Other questionnaires included: a medical history questionnaire, 14-item Resilience Questionnaire 8,9 , and the Satisfaction with Life Scale (SWLS) 10,11 . To assess physical function the short physical performance battery (SPPB) 12 and the timed up and go (TUG) 13 test was used. Assessments took approximately 3 ½ hours to complete per participant.

Anthropometrics
Trained study staffed obtained all measurements using standard procedures.
Height (cm) and weight (kg) were measured using a stadiometer (Webb City, MO, USA). Height was rounded to the nearest 0.5 cm and weight was rounded to the closest 0.1 kg. Height and weight value was used to calculate BMI (kg of body weight/height in meters 2 ). Body mass index was classified according to predetermined categories: underweight <18.5 kg/m 2 , normal weight = 18.5-24.9 kg/m 2 , overweight = 25-29.9 kg/m 2 and obese ≥ 30 kg/m 2 14 .
A foot-to-foot bioelectrical impedance analysis device (Tanita BF-556, Arlington Heights, Illinois) was used to obtain body composition. This is a portable, battery-operated device that uses a very low electrical current (battery powered, 50 kHz) to estimate fat mass and percentage body fat. This test is a valid and reliable tool to measure body composition 15 . According to the American Council on Exercise 16 , any female with ≥32% body fat and any male with ≥25% body fat was considered obese. Even though risk for this test is minimal, participants with a pacemaker were not tested.

Biochemical Markers
Serum total cholesterol, low-density lipoprotein cholesterol (LDL-C), highdensity lipoprotein cholesterol (HDL-C), triacylglycerol (TRG), and glucose were obtained using a finger stick (Cholestech ® LDX system, Hayward California). Prior to obtaining blood markers, participants were instructed to abstain from eating or drinking for 12 hours. However, unlimited water intake was permitted and encouraged during the 12 hour fast. Forty microliters of blood was drawn from the participant's finger by trained personnel using a lancet, collected into a capillary tube, put into a cartridge, and assayed using the portable Cholestech ® (LDX system, Hayward California) machine. The study staff used universal precautions and standardized protocols. Participants with total serum cholesterol <200 mg/dL, LDL-C < 100 mg/dL, HDL-C > 40 mg/dL, and TRG < 150 mg/dL will have a serum lipid panel within normal limits 17 . A clinical diagnosis of high biochemical values include TC >240 mg/dL, HDL-C <40 mg/dL, LDL-C >160 mg/dL, and TRG >200 17 . Fasting blood glucose <100mg/dL was considered normal, 100-125mg/dL impaired, and > 126mg/dL was considered high.

Blood Pressure
Trained study staff measured blood pressures 18 . Participants sat quietly for five minutes and the cuffed arm was supported at heart level. Blood pressure was measured using an automatic blood pressure machine (Omron Healthcare Inc., Bannockburin Illinois). Blood pressure was taken twice or until readings were within 2 mg/dl and the readings were averaged together. Systolic blood pressure <120mmHg and diastolic blood pressure < 80 mmHg were considered within normal limits. Systolic blood pressure > 130 mmHg and diastolic blood pressure > 85 mmHg were considered borderline high, while SBP >140mmHg and DBP >90 mmHg was considered hypertensive.

Questionnaires
Due to cognitive difficulties, the described questionnaires were to chosen to decrease labor intensity for the population of interest. To reduce error and inaccuracy, short questionnaires validated in elderly populations, neurological conditions or physical disabilities were selected.

Cognitive-Linguistic
To measure attention, language, memory, constructional and visual-spatial abilities, the RBANS was used 1 . It includes 12 subtests, with five index scores, summarizing: immediate memory, visuospatial/constructional, language, attention and delayed memory. The total score is the sum of all the index scores. Scoring is based on a mean of 100 and a standard deviation of 15, and a score <70 indicates suboptimal cognitive function. The test takes approximately 30 minutes to complete and is intended to assess adults ages 20-89.

Swallowing Evaluation
The SWAL-QOL is a 44-item survey where participants rate factors about 10 quality of life concepts related to swallowing 2,3 . Specifically, participants were asked how swallowing problems affect their daily lives, especially in regards to eating and diet 2,3 . The highest possible score is 220, the higher the score the better one's swallowing function. The SWAL-QOL took approximately 10 minutes to complete.

Dietary Quality & Nutrition Risk Assessment
Participants completed the DST. This 25-item questionnaire is used to identify dietary patterns and nutritional risk in older adults 4,5 . Participants reported how frequently they consumed a food or type of food, as well as different dietary practices.

Physical Activity Survey
The PADS was used to measure activity level. This survey is a validated and reliable source to measure physical activity in those who are sedentary and disabled 6,19 . This tool covers a wide range of activities and includes six sub-scores: exercise, leisure-time physical activity (LTPA), general activity, therapy, employment, and wheelchair use. Scores increase as physical activity increases. The PADS is coded based on intensity, type and amount of activity, and can detect varying levels of physical activity 19 . Raw scores of 0-27 indicate minimal, 28-42 is minimal to moderate, 43-67 is moderate, and > 68 indicates an extreme level of activity 6 . This survey took about 20 minutes complete.

Physical Functioning Assessment
The SPPB 12 was completed to assess participants' global physical functioning and included timed measures of usual gait speed, standing balance tests, and repeated five chair stands. For the balance tests participants were asked to maintain their feet in side-by-side, semitandem, and tandem stances for 10 seconds each. To assess walking speed participants walked four meters at their usual pace. Walking speed was performed twice, and the faster time was recorded. During the chair test participants stood up from sitting position with their arms folded across their chest. If the participant were able to perform this task, they were instructed to stand up and sit down five times as quickly as possible. The time to perform this task was recorded.
SPPB scores are reported out of 12, and each sub score ranges from zero to four, and the higher the score the better lower physical function. Scores 8-12 are considered "high functioning 12 .
A timed up and go (TUG) test was used to assess basic functional mobility 13 .
It measures the time it takes for the participant to raise from a chair, walk three meters, turn around and walk back to the chair. The shorter amount of time, the better the score. Time was recorded in seconds, the test was administered twice and the better score was recorded. Those with TUG scores >13.5, are considered high risk for falls 20

Past Medical History Questionnaire
To identify health-related conditions and how these conditions may impact health, a non-validated medical history questionnaire will be used. Topics covered will include neurological, endocrine and cardiovascular health. Ten minutes were allotted to recite and complete this survey for each participant.

Resilience
The 14-item Resilience Scale 8,9 measured resiliency. Resiliency is one's ability to recover from a physiological or psychological event 8,9 . It is a validated and reliable tool that has found a significant correlation between resilience, morale, depression and overall life satisfaction in older adults 9 . Questions are answered on a Likert scale from one to seven, where participants reflect on their belief that their life has meaning, sense of uniqueness, and ability to exist alone and manage their lives; higher scores are associated with greater degrees of resiliency 8,9 . It took approximately five minutes to complete. Total possible scores range from 14 to 98, and a higher score indicates higher levels of resilience.

106
The SWLS, a five-item questionnaire, was used to obtain overall life satisfaction 10 . It is used to measure global life satisfaction by asking participants to make a broad judgment of their life 10 . This questionnaire is answered on a Likert scale that ranges from one to seven 10,11 . Total possible score ranges from five to 35, and the higher the score, the greater life satisfaction.

Cardio-Metabolic Assessment
Cardio risk factors were selected, and grouped into eight categories based upon modifiable and non-modifiable risk factors. These eight selected categories included:

Statistical Analysis
This is the first analysis of this study, and therefore statistical analysis were not hypothesis driven, but conducted to generate hypothesis and explore the population. For all normally distributed data, independent t-tests were conducted to determine if there were significant differences between groups regarding assessment variables. Cohen's d was calculated to describe effect size for differences between groups in normally distributed variables (0.2 = small effect, 0.5 = medium effect, 0.8 = large effect). For data not normally distributed, Mann-Whitney U tests were used to analyze differences between groups and effect size was signified through calculating r (0.1 = small effect, 0.3 = medium effect, 0.5 = large effect). Between group differences for categorical variables were identified using Fisher Exact Tests. Phi coefficient or Cramer's V were used to signify effect size (0.1 = small effect, 0,3 = medium effect, 0.5 = large effect). Pearson's R Correlations were used for normally distributed variables, and Spearman Rho Correlations were used as the non-parametric alternative. Significance for all analyses was set at p <0.05.

Power Calculation
An A-priori power analysis found that a sample of 28 PD participants and 14 ABI participants would find significant difference between groups and SPPB scores.
To find significant differences between groups and DST scores, an A-priori power analysis suggests 63 PD participants and 31 ABI participants are needed.

Resources Required
Funding for this research was provided by URI's Department of Communicative Disorders. Supplies provided by the Department of Nutrition and Food Sciences included: computers, printers, computer software, paper and physical assessment equipment. Personnel to conduct the study were supplied by the

Departments of Communicative Disorders, Kinesiology, and Nutrition and Food
Sciences. No other university resources will be required for this study.
included in the study before you decide whether you want to take part in the study. You may also quit the study at any time.

What will be done:
If you agree to take part in this study, you will be asked to complete up to 11 evaluations over five years. Evaluations will take place every six months. The evaluations will include a variety of tasks such as reading sentences and describing a picture, an assessment of how your muscles move, a cognitive screening, an interview, a clinical swallowing evaluation, and questionnaires regarding swallowing, diet and physical activity. The total time for each evaluation will be approximately 3½ hours. All evaluations will be conducted in a quiet private room at one of the University of Rhode Island Speech and Hearing Clinic locations (Kingston or Pawtucket).
With your permission, we will request health information from your physician about the following specific items only:  Date of diagnosis  Current medications  Imaging information about where the brain damage is located (if appropriate) You will sign a separate form to indicate whether you give your permission to release this health information for the study.

Potential risks and discomforts:
There are minimal foreseeable risks associated with these evaluations. There have been no reported adverse affects from clinical evaluation of speech and swallowing. There may be some unknown or unanticipated risks, but every precaution will be taken to ensure your personal safety. Even though experienced personnel will obtain the blood samples from a finger prick, there is a chance of discomfort and minor bruising from the finger stick. For physical function testing there is a risk of muscle soreness or other muscle injury as well as skeletal injury but we will minimize these risks by using standard safety practices.

Purpose and benefits of the study:
The purpose of this study is to describe communication, nutrition, and physical activity behaviors over time to see how they change and affect quality of life. The information obtained is important because it will help us to understand how to provide services to meet the needs of people with neurological diagnoses. This is an investigational study and there is no guaranteed benefit to your communication or nutrition or physical function as a result of participation in this research study. You will receive personal health information such as your height and weight, physical function determined by a physical assessment, your blood lipids such as cholesterol and triglycerides. In addition, you will receive information about your thinking skills and language skills and dietary choices.

Drugs, devices or instruments to be used:
Drugs will not be used in this study. The equipment for the evaluations include: microphone, sound level meter, tongue blade, a digital tuner, tape recorder, and video cameras. All equipment used to collect cognitive-linguistic and physical function data is considered non-invasive. A lancet and capillary tube will be used to obtain the blood sample from a finger prick and the sample will be analyzed on a small portable machine that is on a table.

Cost to participant:
There is no cost to you for participation in the evaluations. Parking is available for free.

Confidentiality:
Your part in this study is confidential. Your individual privacy will be maintained in all published and written data resulting from this study. No names of participants will be published or included in written data resulting from this study. Results of this study may be used for purposes of research, educational lectures, and/or professional presentations. When you are entered into the study you will be assigned a code that does not include any identifying information. For example, the first participant will be coded as Long01. The code number will be used on all response forms and in the analysis of the data.
Dr. Mahler and her research team will have sole access to all contact information and evaluation results containing your name. This information will be kept in a locked filing cabinet in a locked office. However, the U.S. Department of Health and Human Services, and the University of Rhode Island Institutional Review Board have the right to inspect all of your records relating to this research for the purpose of verifying data. Because of the need to release information to these parties, absolute confidentiality cannot be guaranteed. Following completion of this project, contact information will be destroyed for those participants who wish, for any reason, not to be contacted in the future. All other information will be archived and kept in a locked filing cabinet with the study results at the University of Rhode Island. All research data will be retained for a minimum of three years following completion of the study and then will be destroyed. Research data will be located in a locked filing cabinet in the principal investigator's locked office.
Cognitive-linguistic evaluations will be audio and video recorded to allow for data analyses. At times these recordings can be useful for teaching students or professionals about the disorders of people with a neurological diagnosis such as yours. Please indicate by signing below whether you give your permission to use your samples for lectures and presentations. Audio and/or videotapes may be used for teaching for up to 3 years after completion of the study. If you agree, you will never be identified by name in the presentations or lectures. Your decision to give permission to use audio and/or video samples in lectures has no impact on your participation in the study. If you are injured during an evaluation or during treatment every effort will be made to get you medical attention but you will be responsible for paying for the medical treatment needed.

Decision to quit at any time:
The decision to take part in this study is up to you. You do not have to participate. If you decide to take part in the study, you may quit and stop participating in this study at any time. You have the right to refuse to answer any question(s) or participate in any procedure for any reason. Deciding not to participate will have no effect on your potential to receive services from a speech-language pathologist. If you wish to quit, simply inform Leslie Mahler at 874-2490 of your decision. If you wish to pursue an alternative treatment instead of completing the study you will be provided with information on how to obtain those services.

Rights and complaints:
If you are not satisfied with the way this study is performed, you may discuss your complaints with Dr.