I'm working in a 6 page research paper and below is the complete list of the paper has to be set up and the required things needed to be included. Can you check to see what is already included on the list and what is missing in my paper. Also, what I need to improve and how? My topic is "The Struggles of Epilepsy". Can you help me with the content (background, empirical research, and hypothesis )? I also need an operational definition of the independent and dependent variable, but I am having trouble with that. It is due on the 14th. The list below is how my paper must be outlined and the sources I must have. I don't have a hypothesis. The basic idea of my paper is in the title itself and what people with epilepsy have to go through as far as symptoms, personality changes, treatment and ways to support others with epilepsy.
Headings (start your introduction with the title of your study, other headings are not necessary. However if you are using other headings, limit them to 2.
Spacing (double space throughout
Font (use 12 point font, Times New Roman)
Margins (should be 1 inch on all sides)
Quotations: limit to 2 quotes (1 short direct quote and 1 long direct quote)
Page numbering (top right hand corner)
Use correct page format (see below)
Cite any idea, statement, comment, and question, that is not your own.
2. Grammar and Punctuation
This includes all aspects of grammar and punctuation
Proper use of tense (Use past tense but for hypothesis paragraph use future tense).
3. General Writing Style
Flow (no jargon or wordiness; no redundancy; also have transition)
Organization (organized in paragraphs; general organization of a beginning middle, and end)
Clarity (word choice; also avoid the use of first person, do not use the words, prove, proven, proves, proved, or proving)
4. Content
Your design must be experimental
Cite at least 6 sources (3 empirical articles/studies; 3 theoretical, or other for example, book/book chapters). In other words, you need 6 sources (3 empirical and 3 theoretical/review from professional sources)
A. Background
B. Empirical Research Section (research that supports your hypothesis)
C. Hypothesis paragraph (the last paragraph of your introduction should include the following:
5. Length
Your introduction should be at least 3 pages long (this does not include the title page, abstract, or reference list)
Abstract is optional and is extra credit (3 points). The abstract is page 2
6. Page Format
Title page –page 1 (separate page)
Abstract (optional) – page 2 (separate page)
Introduction – page 3
Reference list – possibly page 6 (depends on whether your introduction exceeds 3 pages, should be on separate page).
Here is what I have so far:
My Independent Variable is therapy
Dependent Variable is depression level - score on a BDI
I don't have an operational definition yet. I need one for the IV and DV
The Struggles of Epilepsy
Epilepsy is a neurological condition that affects the brain and nervous system. It is also referred to as “seizure disorder.” Epilepsy can be caused by brain injury, infection, or family genetics. However, the cause in unknown in most causes. Having epilepsy can affect relationships, driving memory, work and more. Imagine if your brain was reset. Imagine not knowing who you are, where you are, or how you got there.
Scary, right? Well, this is what I and other people with epilepsy go through after having a seizure. A seizure is an abnormal discharge of electrical activity in the brain. With epilepsy, you tend to have seizures back to back. For some, seizures are brief and not too threatening, but for others their brain resets itself and leaves the completely powerless with no awareness of what’s going on around them.
Additionally, the cause of all seizures is unclear, but doctors have come up with some reasons why they may occur. Common forms of generalized epilepsy, absence attacks, and tonic-clonic seizures are sometimes caused because of an inherited instability. This is where the inherited instability in functioning of neurons is responsible for these disorders. It is still not understood just how this genetic defect works, it could be the abnormality is in the structure of the neuron’s outer membrane, which could cause electrical instability
Furthermore, as a first step, simple regression analysis were performed with including VNS therapy which was selected as independent variables while BDI-21 and STAI-S and -T were selected as dependent variables as the independent variable. The score on a Beck Depression Inventory (BDI-21) and State-Trait Anxiety Inventory (STAI) scores and was selected as the dependent variable. Subsequently, the most significant of these factors were further investigated with multiple regression analysis. Data concerning age, duration of disease, BDI-21 and STAI were entered in the model as continuous variables, while the variables of gender, epilepsy type and medication were entered in as model variables. The associations between the dependent and independent variables are presented by means of unstandardized linear regression coefficients and 95% confidence intervals.
In addition, all reported associations were ranked according to the absolute value of their standardized effect, which was quantified by the standardized regression coefficients (β). A standardized regression coefficient is defined as a regression coefficient that has the effect of the measurement scale removed so that the size of the coefficient can be interpreted; it is calculated by multiplying the regression coefficient by the ratio of the standard deviation (SDx) of the independent variable to the standard deviation (SDy) of the dependent variable (β = regression coefficient × SDx/SDy).
Epilepsy is usually treated by medications and in some cases by surgery, devices, or dietary changes. Treatment consists of nerve pain medication, anticonvulsants, and sedatives. VNS therapy involves a small electrical device, like a pacemaker, which is implanted under the skin of your chest. The device sends electrical impulses to your brain through a nerve in your neck called the vagus nerve. The aim is to reduce the number of seizures you have and make them less severe.
Struggles of Epilepsy
Epilepsy is a chronic disorder in brain which occurs due to recurrent, unprovoked seizures. A person is diagnosed with epilepsy if they have two unprovoked seizures (or one unprovoked seizure with the likelihood of more) that were not caused by some known and reversible medical condition like alcohol withdrawal or extremely low blood sugar.
The seizures in epilepsy may be related to a brain injury or a family tendency, but often the cause is completely unknown. The word "epilepsy" does not indicate anything about the cause of the person's seizures or their severity.
Epilepsy can be caused by brain injury, infection, or family genetics. However, the cause in unknown in most causes. Having epilepsy can affect relationships, driving memory, work and more. Imagine if your brain was reset. Imagine not knowing who you are, where you are, or how you got there.
Scary, right? Well, this is what I and other people with epilepsy go through after having a seizure. A seizure is an abnormal discharge of electrical activity in the brain. With epilepsy, you tend to have seizures back to back. For some, seizures are brief and not too threatening, but for others their brain resets itself and leaves the completely powerless with no awareness of what’s going on around them.
Additionally, the cause of all seizures is unclear, but doctors have come up with some reasons why they may occur. Common forms of generalized epilepsy, absence attacks, and tonic-clonic seizures are sometimes caused because of an inherited instability. This is where the inherited instability in functioning of neurons is responsible for these disorders. It is still not understood just how this genetic defect works, it could be the abnormality is in the structure of the neuron’s outer membrane, which could cause electrical instability
Some characteristics of epilepsy is given below -
Demographic and epilepsy data questionnaires
1. Dependent variables
The following continuous dependent variables were used in the present study: a) quality of life, measured using Quality of Life in Epilepsy by using questionnaire and Quality of Life in Epilepsy Inventory for Adolescents by using other questionnaire .The 1st questionnaire is made up of 31 questions distributed into seven domains: general quality of life, seizure worry, emotional wellness, energy and fatigue, cognitive function, social functioning and medication effects. On the other hand, 2nd is made up of 48 questions distributed into eight domains: epilepsy impact, memory and concentration, attitude toward epilepsy, physical functioning, epilepsy stigma, social support, scholar behaviour, and health perception. Both instruments generated a continuous total score ranging from zero to 100. The higher the score, the higher the quality of life. This study used only the total score from both questionnaires. b) Side effects: the Adverse Effects Profile (AEP) scale is made up of 19 questions which were answered using a Likert-type scale; individuals with scores ranging from 19 to 76 and individuals above 45 points are considered at higher risk of side effects . c) Depression was measured using the Neurological Disorders Depression Inventory for Epilepsy (NDDI-E) which consists of six questions generating a continuous score ranging from six to 24 points. Scores higher than or equal to 15 indicate a diagnosis of depression; d) Anxiety: the short version of the State–Trait Anxiety Inventory (STAI) was used. The questionnaire is divided in two instruments, one assesses the anxiety status (STAI-S-6) and the other the anxiety traits (STAI-T-6). Each one consists of six questions ranging from six to 24 points. The higher the scores, the higher the state and anxiety traits.
2. Independent variable
To measure physical activity in adolescents and adults, the Physical Activity Questionnaire for Adolescents and the International Physical Activity Questionnaire— long version, were respectively used. The IPAQ measures physical activity levels for a normal week in the domestic, leisure, commuting and work domains. However, this study only used the leisure and commuting domains, as the domestic and work domains seemed overestimated.
In the present study, the physical activity variable was categorized as follows: a) adults — inactive (less than 10 min of physical activity per week), insufficiently active (10 min or more per week and less than 150 min per week) and active (150 min or more of physical activity per week). b) Adolescents: inactive (0 min of physical activity per week), insufficiently active (more than 0 min and less than 300 min per week) and active (300 min or more of physical activity per week). Additionally, to calculate the scores for the IPAQ domains, minutes of vigorous physical activity were multiplied by two. The same process was followed for PAQ-A, in which sports were considered vigorous physical activities and, as a result, the reported time was also multiplied by two. The physical activity scores for leisure and commuting were added. As a cut-off point for the individuals considered active, recommendations from the World Health Organization (WHO) of 300 min of physical activity per week for adolescents and 150 min for adults in a week were used.
3. Ethical procedure
The study was analyzed and approved by the Ethical Committee from the Physical Education College of the Federal University of Pelotas under protocol numbered 1.231.971. The participants of the study were informed of the protocol and provided written consent. For individuals younger than 18 years, the participants' parents signed the consent form.
4. Statistical analysis
Epidata software 3.1 was used to build up a dataset which was double-entered and after checking for error, transfer of the dataset to Stata 13.1 was carried out. Descriptive statistics were used to characterize the sample (mean, standard deviation, median, interquartilic range and relative frequency). To verify the association of physical activity levels according to the control variables, analysis of variance (ANOVA) was used with post-hoc Bonferroni for parametric variables, and Kruskal–Wallis with Dun post-hoc for the non-parametric variables. Categorical variables were analyzed by Chi-squared tests. The visual histogram inspection along with the Shapiro–Wilk test to check the dependent variable normality and the Bartlet test to check variance homogeneity were used. All dependent variables were considered parametric.
Simple linear regression was used for the crude analysis of all dependent variables according to physical activity levels. Adjusted analysis by multiple linear regression was conducted including sociodemographic, clinic, behavioral and health variables which the crude association with each dependent variables was p ≤ 0.05. The variables which were included in the model were removed one at a time (variables with higher p values) up to a point in which all included variables showed a p ≤ 0.2 value. The significance level was set at p < 0.05.
5. Results
The characteristics of the sample study according to physical activity levels are shown in Table 1. Most of the independent variables do not present differences according to physical activity levels. Physical activity was associated with occupation. The active group showed better quality of sleep compared with the inactive and insufficiently active groups.
Table 1General characteristics of people with epilepsy according physical activity levels (n = 101). |
|||||
Characteristics |
Physical activity |
||||
Inactive |
Insufficiently active |
Active |
p value |
||
Age (years) |
35 ± 17 |
32 ± 17 |
31 ± 17 |
0.57α |
|
Schooling (years) |
8 ± 4 |
7 ± 3 |
8 ± 4 |
0.82α |
|
Income (Reais) |
788 (0–1.200) |
788 (400–1.200) |
788 (600–1.200) |
0.66† |
|
Sex (%) |
0.61£ |
||||
Male |
51.4 |
42.9 |
55.6 |
||
Female |
48.7 |
57.1 |
44.4 |
||
Skin color (%) |
0.41£ |
||||
White |
70.2 |
50.0 |
55.6 |
||
Black |
13.5 |
25.0 |
27.8 |
||
Brown |
16.2 |
25.0 |
16.7 |
||
Occupation (%) |
0.01£ |
||||
Student |
13.5 |
32.1 |
44.4 |
||
Employed |
32.4 |
17.9 |
33.3 |
||
Unemployed |
35.1 |
42.9 |
11.1 |
||
Retired |
18.9 |
7.1 |
11.1 |
||
Marital status (%) |
0.13£ |
||||
Single |
46.0 |
60.7 |
69.4 |
||
Married |
43.2 |
21.4 |
22.2 |
||
Widowed |
8.1 |
3.6 |
5.6 |
||
Divorced |
2.7 |
14.3 |
2.8 |
||
Number of children (%) |
0.10£ |
||||
0 |
62.2 |
57.1 |
69.4 |
||
1 |
13.5 |
10.7 |
11.1 |
||
2 |
13.5 |
28.6 |
2.8 |
||
3 or more |
10.8 |
3.6 |
16.7 |
||
Welfare (%) |
0.09£ |
||||
Yes |
27.0 |
32.1 |
11.1 |
||
No |
73.0 |
67.9 |
88.9 |
||
Seizure type (%) |
0.05£ |
||||
Generalized |
26.2 |
28.6 |
45.2 |
||
Focal |
50.0 |
50.0 |
00.0 |
||
Focal secondarily generalized |
57.6 |
21.2 |
21.2 |
||
Unknown |
40.0 |
40.0 |
20.0 |
||
Etiology (%) |
0.04£ |
||||
Idiopathic |
22.7 |
22.7 |
54.5 |
||
Symptomatic |
54.2 |
16.7 |
29.2 |
||
Unknown |
42.1 |
36.8 |
21.0 |
||
Number of seizure during life (%) |
0.58£ |
||||
≤15 seizures |
33.3 |
33.3 |
44.1 |
||
>15 seizures |
66.7 |
66.7 |
55.9 |
||
Duration of epilepsy (%) |
0.81£ |
||||
≤15 years |
48.6 |
53.9 |
57.1 |
||
>15 years |
51.4 |
46.1 |
42.9 |
||
Treatment (%) |
0.07£ |
||||
Monotherapy |
57.6 |
57.1 |
81.3 |
||
Polytherapy |
42.4 |
42.9 |
18.8 |
||
Active epilepsy (%) |
0.14£ |
||||
Yes |
70.3 |
78.6 |
55.6 |
||
No |
29.7 |
21.4 |
44.4 |
||
Seizure control (%) |
0.09£ |
||||
Controlled |
48.6 |
44.0 |
75.0 |
||
Not always controlled |
25.7 |
32.0 |
11.1 |
||
Not controlled |
25.7 |
24.0 |
13.9 |
||
Smoking (%) |
0.44£ |
||||
Never |
59.5 |
78.6 |
69.4 |
||
Ex-smoker |
21.6 |
10.7 |
22.2 |
||
Smoker |
18.9 |
10.7 |
8.3 |
||
Quality of sleep |
8.1 ± 3.2 |
8.3 ± 3.4 |
6.4 ± 2.7a |
0.03α |
|
Stress |
22.1 ± 6.5 |
22.1 ± 7.6 |
19.5 ± 7.2 |
0.26α |
Results are expressed as mean ± SD (parametric variables), median and interquartile range (nonparametric variables) and relative frequency (%) (categorical variables). Statistical tests: analysis of variance with Bonferroni post-hoc (α), Kruskal–Wallis with Dun post-hoc (†) and Chi-squared (£).
a Statistically significant difference between groups (p < 0.05).
Table 2 shows the crude association among dependent and control variables that were taken for regression analysis. Fifteen control variables were associated with quality of life and six variables remain associated after the adjusted regression analysis (skin color, welfare, active epilepsy, smoking, quality of sleep and stress). In the crude analysis, the dependent variable side effect of medication was associated with eight control variables and five variables remained associated after adjusted regression analysis (sex, number of seizures, etiology of seizure, quality of sleep and stress). Depression was associated with eight control variables in the crude analysis and five variables remained associated after adjusted regression analysis (sex, etiology of seizure, active epilepsy, quality of sleep and stress). After crude analysis, the state anxiety variable was associated with 10 control variables and seven variables remained associated (sex, skin color, marital status, schooling, income, quality of sleep and stress) after adjusted regression analysis. Finally, the trait anxiety variable was associated with six control variables and two variables remained associated after adjusted regression analysis (quality of sleep and stress).
6. Discussion
The present study aimed to investigate the association among leisure-time and commuting physical activity levels and several health outcomes (quality of life, medication side effects, depression and state and trait anxiety) in PWE.
6.1. Quality of life
Regarding quality of life, the study shows a linear trend between the groups. The higher the level of physical activity, the higher the quality of life, which increased by 10% for physically active individuals (β = 10.05). A former study by McAuley et al. [22] corroborate with our finding. The authors carried out a randomized clinical trial for 12 weeks with adults with epilepsy divided into two groups: an intervention group (performing physical exercise) and a controlled group (without exercise). The total score for quality of life improved in the intervention group but it was not altered in the control group.
6.2. Depression and anxiety
Results from the present study show associations between physical activity levels and anxiety state and depression, not only in the crude analysis but also in the adjusted one. The trait anxiety did not remain associated after regression analysis. These findings agree with studies previously carried out in PWE [20, 21].
There are several mechanisms supporting the positive changes promoted by physical activity on mental health. These mechanisms are divided into: psychological (distraction, social interaction, self-efficacy, expectations for changes and pleasure in the activities), physiological (thermogenic and brain blood flow), and neurophysiological (monoamines, cerebral lateralization and endorphins) [38]. In this regard, physical activity may have increased endorphin levels and this increase is associated with reduction in anxiety and depression, vigor, wellbeing and increased levels of euphoria[39]. Another explanation for this phenomenon is the monoamine hypothesis which suggests that physical activity level increases the serotonin and norepinephrine levels which are decreased in depressed people, indicating an improvement in humor profile [40, 41].
6.3. Side effects of medication
Regarding the side effects of antiepileptic medication, studies which evaluated the effect of physical activity were not found. The results presented in this study indicate that there was a five point reduction in the total score of side effects for active group individuals. Improvement in quality of life and reduction of medication side effects are in the first and second positions, respectively, according to the caregivers. Therefore, the results are very relevant, considering a positive association between physical activity practice and the
6.4. Limitations
Although there is a biological plausibility of an association between the physical activity and health variables [17, 22], this cross-sectional study is not an ideal design to verify the cause and effect relationship. Another limitation was regarding the instruments used to assess depression, quality of sleep and stress levels, which were validated only for adults and the elderly. However, validated instruments for adolescents which aim at measuring these variables are unknown. As a result, more studies are needed, mainly randomized clinical trials, to establish a more precise relationship between cause and effect.
7. Conclusion
Physical activities, such as, leisure-time and commuting, are associated with health outcomes. The higher the physical activity level, the higher the scores for quality of life in addition to reducing depression, anxiety state and medication side effects scores. To sum up, physical activity regarding the analysed domains may be a no pharmacological treatment to improve health and life conditions of PWE.
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