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Daily Diary
▶Diaries
Daily Hassles
▶Daily Stress
Daily Mood Variation
▶Diurnal Mood Variation
Daily Stress
C. Renn Upchurch Sweeney
VA Salt Lake City Healthcare System, Salt Lake City, UT, USA
Synonyms
Daily hassles;Everyday problems
Definition
Daily stress is defined as mundane hassles, strains, or annoyances associated with routine
daily activities and transactions of everyday life.
Daily stress is relatively minor, but has the potential to disrupt the flow of everyday life and add to overall levels of stress.
Daily stress can be both anticipated and unanticipated. Anticipated daily stressors include, for example, driving in rush hour traffic on the way home from work, paying bills, working long hours, job performance evaluations, or taking children to after-school activities. Unanticipated stressors may include arguments with spouse, car trouble, getting stuck in long lines at the grocery store, getting sick, losing one’s keys, or inconveniences due to weather.
Description
Daily stressors are not inherently stressful events, but they are events that people might appraise as stressful. The experience of feeling stressed depends on what events one notices and how one appraises or interprets these events, which is referred to as the “primary appraisal.” Events that are stressful for one person may be routine for another. For example, one may see an upcoming job interview as an exciting opportunity. Others may view it as terrifying.
Theoretically, the person then engages in a “secondary appraisal” to determine the ade- quacy of personal and social resources for dealing with the stressor.
Daily stress is different from major life stressors such as getting married, death of a loved one, or M.D. Gellman & J.R. Turner (eds.),Encyclopedia of Behavioral Medicine,
DOI 10.1007/978-1-4419-1005-9,#Springer Science+Business Media New York 2013
divorce. Unlike life events that call for people to make adjustments to their lives, daily hassles are part of everyday life. Daily stress is more frequent and continuous form of stress than less frequent events that constitute major life stressors. Because of its frequency it may be a more important deter- minant of stress than major life stressors.
Daily stress and minor hassles have been found to be important forms of stress. Research indicates that routine hassles may have significant harmful effects on mental and physical health (i.e., declines in physical health such as headaches or backaches or worsening of symptoms in those already suffer- ing from illness). Minor hassles can produce stress and aggravate physical and psychological health in several ways. First, the effect of minor stressors can be cumulative. Each hassle may be relatively unimportant in itself, but after a day filled with minor hassles, the effects add up. The cumulative impact of small stressors may wear down an indi- vidual until the person eventually feels overwhelmed, drained, grumpy, or stressed out.
The aggregate effects of everyday hassles have the potential to compromise well-being or predis- pose an individual to become ill. Second, daily stress can contribute to the stress produced by major life stressors and influence the relationship between major life events and illness. That is, daily stress can contribute to the stress produced by major life events. If a major life event is experi- enced at a time when minor life events are also high in number, the stress may be greater than it would otherwise be. Alternatively, major life events, either positive or negative, can also affect distress by increasing the number of daily hassles they create.
References and Readings
Cooper, C. L., & Derre, P. (2007). Stress: A brief history from the 1950s to Richard Lazarus. In A. Monat, R. S.
Lazarus, & G. Reevy (Eds.),The Praeger handbook on stress and coping (2007th ed., Vol. 1, pp. 7–31).
Westport, CT: Greenwood Publishing.
Kohn, P. M. (1996). On coping adaptively with daily hassles. In M. Zeidner & N. S. Endler (Eds.), Handbook of coping: Theory research, & applications (pp. 181–201). Oxford, England: Wiley.
Taylor, S. (2006).Health psychology(6th ed.). New York:
McGraw-Hill.
Weiten, W. (1995). Themes and variations (3rd ed.).
Pacific Groove, CA: Brooks/Cole.
Dangerous Drinking
▶Binge Drinking
Data
J. Rick Turner
Cardiovascular Safety, Quintiles, Durham, NC, USA
Synonyms
Numerical information; Numerical representa- tion of (biological, psychological, behavioral) information
Definition
Data is a plural construct indicating more than one piece of numerical information. The singular form of the term is datum. Statistical analysis (certainly of the type useful in the discipline of behavioral medicine) almost always uses more than one piece of numerical information, and the term datum does not occur again in any other methodology entry in this encyclopedia.
Description
Accordingly, plural words are used in conjunc- tion with the word data: “the data are, the data were, these data, the data show, etc.” If you are uncertain as to how to construct a phrase includ- ing the word data, replace the word data in your mind with the word results. While the terms data and results are not truly synonymous, the word results is also a plural construct. This strategy will
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538 Dangerous Drinkingtherefore likely help you express a phrase includ- ing the word data correctly.
Data can generally be classified into one of the following scales of measurement: nominal, ordi- nal, and ratio. Nominal scales involve names of characteristics. Common examples from behav- ioral medicine include sex (male and female sub- jects in a research study) and race or ethnicity. An ordinal scale is defined as one in which an order- ing of values can be assigned. Age of study sub- jects categorized as less than 25 years of age, 25–30 years of age, and 31 years of age and older is one example. Data measured on a ratio scale can be manipulated in certain ways not possible with the previous scales. For example, someone weighing 220 pounds (lbs) can be said to weigh twice as much as another subject weighing 110 lbs. The same applies for height and age. The feature of the ratio scale that makes such comparisons possible is that the value of zero on the scale represents a true zero – a weight of zero and a height of zero (no matter what the unit of measurement) means that there is no weight or height, respectively.
You may have noticed what appears to be an initial contradiction in the previous paragraph:
Age is discussed in both the ordinal scale and the ratio scale discussions. The reason for this apparent paradox is that data can be measured (recorded) on one scale but reported on another.
Imagine that 100 subjects participate in a research study, and each of their ages is recorded in years and months. Then, for various reasons, the subjects are each placed into one of three ordinal categories: those aged less than 25 years of age, 25–30 years of age, and 31 years of age and older. This is perfectly acceptable, but any statistical analysis performed would have to take into account the scale on which the data are reported: Different analyses are appropriate for different kinds of data.
It is also of interest to note that, while it may be convenient to report the subjects’ ages in this ordinal fashion, a certain degree of preci- sion in the information is lost. For example, two subjects aged 26 and 29 years, respectively, would both be placed in the middle category.
Therefore, although they provide different raw
data (their age in years and months) they contrib- ute equally to the total number of subjects in that category.
Cross-References
▶Efficacy
▶Sample Size Estimation
Database Development and Management
J. Rick Turner
Cardiovascular Safety, Quintiles, Durham, NC, USA
Definition
The goal of experimental methodology and oper- ational execution in behavioral medicine research, like all research, is to provide optimum quality data for subsequent statistical analysis and interpretation. These data need to be stored and managed. Databases facilitate such storage and management. Data management is therefore an important intermediary between data acquisi- tion and data analysis.
Description
Analysis of data collected in behavioral medicine clinical trials is typically conducted using files of data contained in a database. It is of critical importance that the data collected from all sources are accurately captured in the database.
A brief list of such data includes: subject identi- fiers (rather than their names); age, sex, height, and weight; questionnaire data concerning a multitude of topics; and physiological measure- ments made before, during, and possibly after the treatment period(s).
A data management plan for a clinical trial is written along with the study protocol and possi- bly a statistical analysis plan before the study
Database Development and Management 539
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commences (statistical details can also be included in the study protocol). The data man- agement plan identifies the documentation that will be produced as a result of all of the data collected during the conduct of the trial. This plan covers items such as:
• The form(s) on which raw (source) data will be recorded.
• Entering data.
• Cleaning the data.
• Creating data reports.
• Transferring data.
• Quality assurance processes.
The quality assurance (QA) component is vital. While differing definitions of quality activ- ities can be found, Prokscha (2007) defined qual- ity assurance (QA) as a process involving the prevention, detection, and correction of errors or problems, and quality control (QC) as a check of the process. The data stored in the database need to be complete and accurate. Processes that check data and correct them where necessary (i.e., make a change to the database) need to be formalized, and all corrections documented in an audit trail such that a later audit can reveal exactly how the final database was created. That is, following initial data entry, the audit trail will record
“who, what, when, why” information for all changes subsequently made.
Having collected optimal quality data, first-rate data management is also critical. Many data that are collected can now be fed directly from the measuring instrument to computer databases, thereby avoiding the potential of human data entry error. However, this is not universally true.
Therefore, careful strategies have been developed to scrutinize data as they are entered. The double- entry method requires that each data set is entered twice (usually by different operators) and that these entries are compared by a computer for any discrepancies. This method operates on the pre- mise that two identical errors are probabilistically very unlikely, and that every time the two entries match the data are correct. In contrast, dissimilar entries are identified, the source data located, and the correct data point entry confirmed.
To facilitate the eventual statistical analysis of the enormous amount of data acquired during a
clinical trial, recording and maintaining them is extremely important. Database development, implementation, and maintenance therefore require attention. The goals of a database are to store data in a manner that facilitates prompt retrieval while not diminishing their security or integrity.
There are several types of database models.
Clinical research typically utilizes one of two types, the flat file database or the relational data- base. Each has its advantages and disadvantages, and these will be considered by data managers before they decide which type to employ. The flat file database model is simple but restrictive, and it becomes less easy to use as the amount of data stored increases. This model can also lead to data redundancy (the same information, e.g., a subject’s birth date, being entered multiple times) and consequently to potential errors.
This model works well for relatively small databases.
Relational databases are more flexible, but they can be complex, and careful initial work is needed. This work involves initial logical model- ing of the database. The defining feature of a relational database is that data are stored in tables, and these tables can be related to each other. This reduces data redundancy. Subject identifiers in one table, for example, can be related to their heights in another table, their baseline blood pressure in another table, and so on, thereby eliminating the need to store identi- fiers with each individual set of measurements.
Since these databases can contain huge amounts of tables, use of one of several commercially available relational database management sys- tems is typical.
Cross-References
▶Study Protocol
References and Readings
Prokscha, S. (2007).Practical guide to clinical data man- agement(2nd ed.). Boca Raton, FL: Taylor & Francis.
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540 Database Development and ManagementDean Ornish
▶Ornish Program and Dean Ornish
▶Preventive Medicine Research Institute (Ornish)
Death
▶Mortality
Death Anxiety
Chad Barrett
Department of Psychology, University of Colorado Denver, Denver, CO, USA
Synonyms
Fear of Death;Thanatophobia
Definition
Death anxiety refers the fear of and anxiety related to the anticipation, and awareness, of dying, death, and nonexistence. It typically includes emotional, cognitive, and motivational components that vary according to a person’s stage of development and sociocultural life expe- riences (Lehto & Stein,2009). Death anxiety is associated with fundamental brain structures that regulate fight-or-flight responses and record emo- tionally charged explicit and implicit memories (Panksepp,2004). Cognitive dimensions of death anxiety can include an awareness of the salience of death and a variety of beliefs, attitudes, images, and thoughts concerning death, dying, and what happens after death (Lehto & Stein, 2009). Death anxiety can be experienced con- sciously or unconsciously; it can motivate indi- viduals to ameliorate their death anxiety through distraction (Greenberg, Pyszczynski, Solomon, Simon, & Breus, 1994), attempts to enhance
self-esteem (Bassett,2007), or by pursuing posi- tive life changes (Tedeschi & Calhoun, 2004).
Individuals experiences of death anxiety can be influenced by their developmental stage. Young adults are mostly concerned about dying too soon, and adult parents are mostly concerned about the effect of their possible death on other family members. Elderly adults are often more concerned with becoming a burden on others, dying alone, or dying among strangers (Kastenbaum, 2000). Sociocultural influences can also shape the cognitive, experiential, and emotional components of death anxiety (K€ubler- Ross,2002; Lehto & Stein,2009).
Description
Most people report some fear of death, but only a few people report high levels of death anxiety (Kastenbaum,2000). According to Noyes et al.
(2000), only 3.8% of respondents indicated that they were much more nervous than most people about death or dying, and 9.8% indicated they were somewhat more nervous than most people.
Stressful experiences can often increase a person’s level of death anxiety, (e.g., life-threatening encounters, tragedies, disasters, health problems, illness, or death of a friend or family member, etc.) (Kastenbaum). A meta-analysis of research on death attitudes among older adults indicated that health problems were associated with elevated levels of death anxiety (Fortner & Neimeyer, 1999). In a later review of the literature on death attitudes, Neimeyer, Wittkowski, and Moser (2004) noted that the relationship between death anxiety and health problems is sometimes equiv- ocal. While many studies found positive associa- tions between health problems and death anxiety, others found no significant relationship. Neimeyer et al. discussed more sophisticated studies and that such conflicting findings may be the result of moderator variables such as social support, coping styles, and religious beliefs. Increased social sup- port, approach- and acceptance-based coping strategies, intrinsic religiosity, and beliefs in a positive afterlife are typically associated with less death anxiety.
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Cross-References
▶End-of-Life Care
▶Palliative Care
References and Readings
Bassett, J. A. (2007). Psychological defenses against death anxiety: Integrating terror management theory and Firestone’s separation theory. Death Studies, 31, 727–750.
Fortner, B. V., & Neimeyer, R. A. (1999). Death anxiety in older adults: A quantitative review.Death Studies, 23, 387–411.
Greenberg, J., Pyszczynski, T., Solomon, S., Simon, L., &
Breus, M. (1994). Role of consciousness and accessi- bility of death-related thoughts in mortality salience effects.Journal of Personality and Social Psychology, 67, 627–637.
Kastenbaum, R. (2000).The psychology of death(3rd ed.).
New York: Springer.
K€ubler-Ross, E. (2002).On death and dying: Questions and answers on death and dying; on life after death.
New York: Quality Paper Book Club.
Lehto, R. H., & Stein, K. F. (2009). Death anxiety:
An analysis of evolving concept.Research and Theory for Nursing Practice: An International Journal, 23, 23–41.
Neimeyer, R. A., Wittkowski, J., & Moser, R. P. (2004).
Psychological research on death attitudes: An over- view and evaluation.Death Studies, 28, 309–340.
Noyes, R., Jr., Hartz, A. J., Doebbeling, C. C., Malis, R. W., Happel, R. L., Werner, L. A., et al. (2000).
Illness fears in the general population.Psychosomatic Medicine, 62, 318–325.
Panksepp, J. (2004).The foundations of human and animal emotions. New York: Oxford University Press.
Tedeschi, R. G., & Calhoun, L. G. (2004). Posttraumatic growth: Conceptual foundations and empirical evidence.Psychological Inquiry, 15, 1–18.
Death Rate
▶Mortality Rates
Death, Assisted
▶Euthanasia
Death, Sudden
Ana Victoria Soto1and William Whang2
1Medicine – Residency Program, Columbia University Medical Center, New York, NY, USA
2Division of Cardiology, Columbia University Medical Center, New York, NY, USA
Synonyms
Sudden cardiac death
Definition
Death within 1 h of the onset of acute symptoms.
Description
Sudden cardiac death (SCD) is an important public health problem, with an annual incidence estimated between 180,000 and 250,000 cases in the United States. The working definition of SCD is death within 1 h of the onset of symptoms, in the absence of preceding evidence of severe pump failure. In prior decades, the majority of SCD cases have been estimated to occur due to rapid cardiac arrhythmia, specifically ventricular tachycardia (VT) and ventricular fibrillation (VF). More recent data indicate that VT/VF is the presenting rhythm in SCD about 30–40% of the time. SCD may also occur due to life- threatening slow heart rhythms (bradycardia) or due to other causes such as massive pulmonary embolism or intracranial hemorrhage (Hinkle &
Thaler,1982; Lloyd-Jones et al.,2010).
In prospective cohort studies, women have a lower incidence of sudden death than men.
Coronary artery disease (CAD) is the most com- mon finding in SCD and is discovered in as many as 80% of SCD cases. However, among the large population of patients with coronary artery dis- ease, the absolute risk of SCD is still low. In addition, a substantial proportion of SCDs occur in the absence of known prior heart disease.
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542 Death RateClinical risk factors for SCD have been devel- oped, and the most reliable of which is reduced left ventricular ejection fraction by cardiac imag- ing such as echocardiogram. However, the prevailing clinical indicators of risk are still lim- ited in their specificity, and identification of indi- viduals at high risk remains a major challenge (Chugh et al.,2008).
Two major mechanisms have been implicated in SCD in the setting of CAD. First, acute plaque rupture may lead to coronary artery occlusion, inadequate blood flow to cardiac muscle (ische- mia), and subsequent VT and VF. Another poten- tial mechanism related to CAD results from the presence of myocardial scar from a prior myocar- dial infarction. With this myocardial substrate, heterogeneity in depolarization and conduction can allow for the development of reentry, in which a tachycardia circuit develops and which manifests as VT that can eventually degenerate to VF. Other underlying cardiac abnormalities can also predispose to SCD. For instance, cardiomy- opathies due to causes other than CAD (e.g., alcohol, long-standing hypertension, sarcoidosis) are also associated with SCD. In addition, pri- mary electrical abnormalities, such as inherited ion channel disorders, are relatively rare but potent causes of sustained ventricular arrhythmia in the absence of structural heart disease (Virmani, Burke, & Farb,2001).
The major treatment against SCD is a preven- tive therapy, the implantable cardioverter- defibrillator. Randomized controlled trials of primary prevention ICD therapy have demon- strated survival benefit in patients with left ventricular ejection fraction <0.36 and with symptoms of congestive heart failure (Bardy et al.,2005; Moss et al.,2002).
A number of studies have noted an association between psychosocial factors, in particular depression, and SCD. For instance, Empana et al. examined data from enrollees of a health maintenance organization in Washington state, in a case control study involving 2,228 out-of- hospital cardiac arrests. Cases of out-of-hospital cardiac arrest (n¼2,228) among patients aged 40–79 years were identified from emergency medical service incident reports, and their
ambulatory medical records were examined for the existence of depression. Compared with nondepressed subjects, the adjusted odds ratio of cardiac arrest was increased in less severely depressed subjects (OR 1.30, 95% CI 1.04–1.63) and further increased in severely depressed (OR 1.77, 95% CI 1.28–2.45) (Empana et al.,2006).
In a cohort analysis involving 915 individuals aged 70 years or older in northern Finland, Luukinen et al. found that depression was asso- ciated with increased risk of sudden death (HR 2.74, 95% CI 1.37–5.50), whereas the risk of non- sudden death was not significantly increased.
(Luukinen, Laippala, & Huikuri, 2003) In the Nurses’ Health Study of 63,000 female nurses without known cardiovascular disease at study outset, cohort analyses indicated a significant association between depression and SCD in mul- tivariable models that included hypertension, dia- betes, and hypercholesterolemia (HR 2.33, 95%
CI 1.47–3.70). The relationship of depression at study outset to subsequent SCD appeared to be related to a specific association with antidepres- sant use (Whang et al.,2009). A separate cohort analysis of the Nurses’ Health Study included 72,359 women with no history of cardiovascular disease or cancer in 1988 and used the Crown- Crisp Index to assess phobic anxiety. During 12 years of follow-up, women who scored 4 or greater on the CCI were at higher risk of SCD (HR 1.59, 95% CI 0.97–2.60). After adjustment for possible intermediaries (hypertension, diabetes, and elevated cholesterol), a trend toward increased risk persisted for SCD (P¼0.06) (Albert, Chae, Rexrode, Manson, & Kawachi,2005).
Cross-References
▶Sudden Cardiac Death
References and Readings
Albert, C. M., Chae, C. U., Rexrode, K. M., Manson, J. E.,
& Kawachi, I. (2005). Phobic anxiety and risk of coronary heart disease and sudden cardiac death among women.Circulation, 111(4), 480–487.
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Bardy, G. H., Lee, K. L., Mark, D. B., Poole, J. E., Packer, D. L., Boineau, R., et al. (2005). Amiodarone or an implantable cardioverter-defibrillator for conges- tive heart failure. The New England Journal of Medicine, 352(3), 225–237.
Chugh, S. S., Reinier, K., Teodorescu, C., Evanado, A., Kehr, E., Al Samara, M., et al. (2008). Epidemiology of sudden cardiac death: Clinical and research impli- cations.Progress in Cardiovascular Diseases, 51(3), 213–228.
Empana, J. P., Jouven, X., Lemaitre, R. N., Sotoodehnia, N., Rea, T., Raghunathan, T. E., et al. (2006). Clinical depression and risk of out-of-hospital cardiac arrest.
Archives of Internal Medicine, 166(2), 195–200.
Hinkle, L. E., Jr., & Thaler, J. T. (1982). Clinical classifi- cation of cardiac deaths.Circulation, 65, 457–464.
Lloyd-Jones, D., Adams, R. J., Brown, T. M., Carnethon, M., Dai, S., De Simone, G., et al. (2010). Executive summary: Heart disease and stroke statistics–2010 update: A report from the American Heart Association.
Circulation, 121(7), 948–954.
Luukinen, H., Laippala, P., & Huikuri, H. V. (2003).
Depressive symptoms and the risk of sudden cardiac death among the elderly. European Heart Journal, 24(22), 2021–2026.
Moss, A. J., Zareba, W., Hall, W. J., Klein, H., Wilber, D. J., Cannom, D. S., et al. (2002). Prophylac- tic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction.
The New England Journal of Medicine, 346(12), 877–883.
Virmani, R., Burke, A. P., & Farb, A. (2001). Sudden cardiac death.Cardiovascular Pathology, 10, 211–218.
Whang, W., Kubzansky, L. D., Kawachi, I., Rexrode, K. M., Kroenke, C. H., Glynn, R. J., et al.
(2009). Depression and risk of sudden cardiac death and coronary heart disease in women: Results from the Nurses’ Health Study. Journal of the American College of Cardiology, 53(11), 950–958.
Decision Analysis
▶Clinical Decision-Making
Decision Authority
▶Job Demand/Control/Strain
Decision Latitude
▶Job Demand/Control/Strain
Decision Making
▶Clinical Decision-Making
Deep Sleep
▶Slow-Wave Sleep
Defense Mechanism
▶Denial
Defensive Coping
▶Defensiveness
Defensive Denial
▶Defensiveness
Defensiveness
Carolyn Korbel1and Sonia Matwin2
1The Neurobehavioral Clinic and Counseling Center, Lake Forest, CA, USA
2Department of Psychiatry, Harvard Medical School, Boston, MA, USA
Synonyms
Avoidant coping; Defensive coping; Defensive denial;Repression;Repressive coping
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544 Decision AnalysisDefinition
Defensiveness is defined as a coping strategy that is characterized by a general orientation away from threatening self-relevant information and a denial or minimization of negative affects such as distress, anxiety, or anger.
Description
Defensiveness is characterized by a general orientation away from threatening self-relevant information and a denial or minimization of negative affects such as distress, anxiety, or anger (Weinberger, Schwartz, & Davidson, 1979). Self-relevant information that is perceived as being inconsistent with personal goals and beliefs is likely to trigger defensive coping reac- tions (Croyle, Sun, & Hart,1997). Defensiveness appears to occur normatively in response to self- relevant health risk information, but also to vary across individuals as a more enduring orientation to coping with distress. There is much conceptual overlap between defensiveness, repressive cop- ing, avoidant coping, and denial in the literature, in that each share a core coping process of min- imizing, denying, or repressing distress, negative affect, or distressing information to serve emo- tion regulation goals (Myers,2010).
Defensiveness has been most frequently assessed through the use of measures of self-reported defensiveness (Weinberger et al., 1979), such as the Marlowe-Crowne Social Desirability Scale (MCSD; Crowne & Marlowe, 1960). Those who score high on social desirabil- ity are thought to minimize, deny, or repress negative emotions such as anxiety and anger, reflecting a defensive or self-deceptive orientation to the self that involves avoidance of distress-arousing thoughts. Measures of self-reported trait anxiety are also frequently used in conjunction with the MCSD to identify those who minimize or deny negative affects and who score high on defensiveness to capture a true defensive or, interchangeably, repressive coping group (Myers, 2010; Weinberger et al., 1979).
Those who have a defensive or repressive coping
style are less likely to report negative affect, distress, somatic symptoms, and chronic stress across a variety of tasks, experimental conditions, and self-report measures. Although defensive/repressive copers deny distress in response to stressful experimental conditions, physiological indicators of distress are often observed.
Defensiveness occurs rather frequently in the population. It has been estimated that 10–20% of the general population, 30–50% of those with particular chronic illnesses, and up to 50% of the elderly use defensive or repressive coping strategies (see Myers,2010for a review). In the context of behavioral medicine, defensiveness appears to prompt cognitive, behavioral, and physiological variations, which may have important implications for health. Specifically, the current literature suggests that:
1. Defensiveness is associated with information processing variations that occur normatively in response to self-relevant health threat information.
2. Defensiveness may have direct effects on physiological functioning.
3. Defensiveness is associated with greater morbidity and mortality in a number of chronic illnesses and disease states.
Defensive Cognitive Processing
Defensiveness influences the way that informa- tion is processed when threatening self-relevant information is perceived. Defensive cognitive processing variations appear to occur norma- tively in response to perceiving personally threat- ening health risk information. Defensive denial processes tend to appear early in the health-threat appraisal process and tend to diminish over time.
They are less extreme when individuals are aware of direct actions to eliminate the threat, and are less common when positive states and experiences (e.g., positive mood, optimism, self-affirmation) are bolstered prior to threat perception, or when active coping alternatives are available and reasonable to execute.
Defensive cognitive processing variations such as (a) minimization of the seriousness of health threats, (b) self-serving prevalence estimates,
Defensiveness 545
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(c) tendencies to denigrate the accuracy or valid- ity of an undesirable test result, and (d) biased processing of health risk information occur frequently in response to perceived health-threat information. These normative defensive pro- cesses may play an important role in regulating emotional distress in the short term so that rational health-protective actions can be identified, enacted, and maintained (Croyle et al.,1997; Wiebe & Korbel,2003).
Physiological Effects of Defensiveness
An emerging literature has identified links between a generalized defensive or repressive coping style and physiological variations in responding which may have direct impacts on health (see Myers, 2010 for a review). It has been hypothesized that the effort required to repress, minimize, or deny negative thoughts and emotions characteristic of defensive coping may result in heightened autonomic reactivity and may impact cardiovascular arousal. Defen- siveness has been associated with increased cardiovascular reactivity to stress via increased sympathetic demand when defensive processes are initiated and maintained. Homeostatic changes in baseline cardiovascular functioning are thought to occur over time in response to increased sympathetic reactivity. Cardiovascular disease risk may be increased in defensives through a physiological mechanism of increased stress reactivity, possibly triggering changes in vascular functions or structure that may alter resting blood pressure levels.
Increased Prevalence of Morbidity and Mortality among Defensive Copers
There is an extensive body of literature that links trait-like defensive and repressive coping with poor physical health (see Myers et al.,2007for a comprehensive review). Repressive/defensive coping appears to both contribute to poor health and disease progression, and to also be used more frequently among those with chronic illnesses.
There is a fairly extensive literature linking repressive coping with increased risk for mortal- ity in coronary heart disease (CHD) and myocar- dial infarction (MI). Repressive coping is
associated with a twofold increased risk of death, MI, and other cardiac events. In addition, heightened levels of defensiveness are associated with hypertension, high blood pressure, as well as high lipid and glucose levels. For example, high scores on the MCSD have been associated with elevated blood pressure and heart rate reactivity.
Additional support for the association between defensiveness and elevated blood pressure in the general population was found in Jorgensen, Johnson, Kolodziej, and Schreer (1996) meta-analysis. Further, a meta-analysis by Mund and Mitte (2011) suggested that repressive copers are at greater risk of developing cancer and coronary heart disease.
Cross-References
▶Cancer Risk Perceptions
▶Cognitive Distortions
▶Coping
▶Defensive Coping
▶Denial
▶Health Behaviors
▶Repressive Coping
References and Readings
Crowne, D. P., & Marlowe, D. (1960). A new scale of social desirability independent of psychopathology.
Journal of Consulting Psychology, 24(4), 349–354.
Croyle, R. T., Sun, Y., & Hart, M. (1997). Processing risk factor information: Defensive biases in health-related judgments and memory. In K. Petrie & J. Weinman (Eds.), Perceptions of health and illness: Current research and applications (pp. 267–290). London:
Harwood Academic.
Jorgensen, R. S., Johnson, B. T., Kolodziej, M. E., &
Schreer, G. E. (1996). Elevated blood pressure and personality: A meta-analytic review. Psychological Bulletin, 120(2), 293–320.
Mund, M., & Mitte, K. (2011). The costs of repression:
A meta-analysis on the relation between repressive coping and somatic diseases. Health Psychology.
doi:10.1037/a0026257. Nov 14, 2011 (No pagination specified).
Myers, L. (2010). The importance of the repressive coping style: Findings from 30 years of research. Anxiety, Stress, and Coping, 23(1), 3–17.
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546 DefensivenessMyers, L., Burns, J. W., Derakshan, N., Elfant, E., Eysenck, M. W., & Phipps, S. (2007). Current issues in repressive coping and health. In J. Denollet, I.
Nyklicek, & A. Vingerhoets (Eds.),Emotion regula- tion: Conceptual and clinical issues(pp. 69–86). New York: Springer.
Weinberger, D. A., Schwartz, G. E., & Davidson, R. J.
(1979). Low-anxious, high-anxious and repressive coping styles: Psychometric patterns and behavioral responses to stress.Journal of Abnormal Psychology, 88, 369–380.
Wiebe, D. J., & Korbel, C. (2003). Defensive denial, affect, and the self-regulation of health threats. In L.
Cameron & H. Leventhal (Eds.),The self-regulation of health and illness behavior(pp. 184–203). New York:
Harwood Academic.
Degenerative Diseases: Disc or Spine
Daniel Gorrin
Department of Physical Therapy, University of Delaware, Newark, DE, USA
Definition
The intervertebral disc is a structure located between adjacent vertebral bodies that functions primarily as a shock absorber. The disc is com- prised of a fibrocartilaginous outer layer called the annulus fibrosus and a gelatinous inner layer called the nucleus pulposus (made up of collagen fibrils embedded within a water/
mucopolysaccharide mix). The disc is connected to the cartilaginous end plates located on the cranial and caudal aspects of the vertebral bodies.
The end plates assist in providing the disc with nutrients.
Degenerative disc disease is a potential cause of back pain marked by an atraumatic, gradual onset of symptoms. Due to its primary function as a shock absorber, the disc is subject to significant
“wear and tear” during the course of a lifetime.
As the patient increases in age, the disc may undergo a degenerative process in which water is lost from the nucleus pulposus and replaced with fibrocartilage. Systemic, cellular, and biochemical changes related to aging may also contribute to degeneration of the disc. Pain
resulting from degenerative disc disease is thought to be caused by a combination of irrita- tion of the disc’s nociceptive fibers and inflam- matory products found within the damaged disc.
The degenerative process can also affect the outer layer of the disc, the annulus fibrosis, which could increase the risk of a herniation of the nucleus pulposus. Tears in the annulus or degen- eration of the annulus can limit the structure’s ability to contain the gel-like nucleus. Release of the nucleus can cause impingement and irrita- tion of the surrounding spinal nerve roots or even the spinal cord itself. This condition (commonly referred to as a “bulging” or “herniated” disc) can result in localized pain at the site of the herniation or pain in the areas supplied by the nerve (radiculopathy).
Patients who experience degenerative disc disease or a disc herniation are likely to regain full function with non-operative treatment. Phys- ical therapy interventions including mobilization, manipulation, traction, core stabilization exer- cises, electrical stimulation, and biofeedback are used in treatment of these conditions. Appropri- ate pharmacological intervention, nerve root injections, and epidural injections can also help provide pain relief. Operative treatment may be indicated if the patient presents with severe neurological deficits or receives no benefit from conservative treatment.
References and Readings
Boyling, J. D., & Palastanga, N. (1994).Grieve’s modern manual therapy (2nd ed.). New York: Churchill Livingstone.
Drake, R. L., Wayne Vogl, A., & Mitchell, A. W. M.
(2010). Gray’s anatomy for students (2nd ed.).
Philadelphia: Churchill Livingstone Elsevier.
Magee, D. J., Zachazewski, J. E., & Quillen, W. S. (2009).
Pathology and intervention in musculoskeletal reha- bilitation(1st ed.). St. Louis, MO: Saunders Elsevier.
McGill, S. (2002).Low back disorders: Evidence based prevention and rehabilitation(1st ed.). Champaign, IL: Human Kinetics.
Yue, J. J., Guyer, R. D., Johnson, J. P., Khoo, L. T., &
Hochschuler, S. H. (2011).The comprehensive treat- ment of the aging spine: Minimally invasive and advanced techniques(1st ed.). Philadelphia: Elsevier Saunders.
Degenerative Diseases: Disc or Spine 547
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Degenerative Diseases: Joint
Beth Schroeder
University of Delaware, Newark, DE, USA
Synonyms
Chronic inflammatory polyarthritis;RA
Definition
Rheumatoid arthritis (RA) is a chronic inflamma- tory condition that affects the synovium of joints in the body. While the exact cause of RA is unknown, it is considered to be an autoimmune condition, in which the body attacks its own healthy cells. In a normal, healthy joint, the syno- vial membrane provides synovial fluid that functions to reduce friction and lubricate the joint surfaces and to provide nutrients to the car- tilage. With RA, the synovial membrane becomes inflamed and thickens, forming a pannus.
A pannus is an accumulation of tissue that ulti- mately causes damage to structures in the joint capsule, such as the cartilage, subchondral bone, and even ligaments.
RA presents with periods of both exacerbation and remission. The typical signs and symptoms of RA include pain, morning stiffness, swelling, and decreased mobility of the affected joints.
Normally, multiple joints are affected in a symmetric pattern, with both sides of the body being affected. The small joints of the hands and feet are the most common joints to be affected, as well as the cervical spine. As the condition progresses, laxity in the ligaments supporting the joint may develop, causing joint deformities or dislocations.
RA’s symptoms are not only musculoskeletal, but the condition can also affect the cardiovascu- lar, renal, and pulmonary systems that may also present in this condition, including fatigue, loss of appetite, and decreased endurance. In some patients, firm skin nodules may form in areas
such as the elbows or fingers. It usually presents between the ages of 20–50 years old, and females are more affected.
Although there is no cure for RA, there are pharmacotherapy treatment options that target the pain and inflammation with hopes of slowing the progressive of the disease. The use of medications includes analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), corticoste- roids, disease-modifying antirheumatic drugs (DMARDS), and biologic response modifiers (BMRs). Physical therapy is also a critical com- ponent in the management of RA. During periods of an active flare, joint protection and rest are the most important. Exercise, though, should still be a component of treatment, organized into short bouts with frequent rest periods to limit fatigue.
In order to prevent deformations and maintain adequate range of motion, it is very important that patients consistently change positions of the affected joints. If swelling is not present, it is also recommended that light stretching be done.
Because the manifestations of RA are irrevers- ible, management and treatment of RA is a lifelong process. It is essential for patients to work closely with their health care providers in order to establish an individualized treatment plan in order to maintain as much functional independence as possible.
References and Readings
A.D.A.M. Medical Encyclopedia [Internet].Rheumatoid arthritis. Atlanta, GA: A.D.A.M.; #2010. [Last reviewed February 07, 2010; cited April 18, 2011];
[about 6 p.]. Retrieved from http://www.ncbi.nlm.
nih.gov/pubmedhealth/PMH0001467/
Goodman, C. C., & Fuller, K. S. (2009).Pathology: Impli- cations for the physical therapist(3rd ed.). St. Louis, MO: Saunders Elsevier.
Kisner, C., & Colby, L. A. (2002).Therapeutic exercise.
Philadelphia: F.A. Davis Company.
Degenerative Parkinsonism
▶Parkinson’s Disease: Psychosocial Aspects
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548 Degenerative Diseases: JointDegrees of Freedom
J. Rick Turner
Cardiovascular Safety, Quintiles, Durham, NC, USA
Definition
Degrees of freedom may be defined as the number of squares of deviations from the mean minus the number of independent linear restric- tions placed upon the quantities involves. Forn numbers there are n squares of deviations from the mean, of which only (n1) are independent.
That is, when (n1) are specified, thenth is also specified.
Description
This is the most esoteric definition in the Methodology category of entries, and please do not be concerned if it sounds a little hard to digest. The following scenario will make it much clearer.
Suppose you are asked a question: “Choose any five numbers that add up to 100.” How much choice do you actually have? A few moments’
thought will reveal that you only have four choices. You can choose any four numbers you wish, but having done so, you have no choice about the fifth. Whatever the sum of the four numbers you have chosen, only one number will take you from there to 100, and hence you have no choice.
Now consider this issue in a slightly different way, but one that is precisely equivalent:
“Choose any five numbers that have a mean of 20.” This is an equivalent task since any five numbers that have a mean of 20 will add up to 100. Therefore, once again, there are only four choices: These four choices precisely determine the value that must be chosen as the fifth. Hence, in a group of scores with a fixed mean, there is one less degree of freedom than the total number
of scores. This explanation ties in to the informa- tion provided in the entry titled “▶Variance,” in which the calculation of variance from a term called “the sum of squares” is described: Vari- ance is obtained by dividing the sum of squares by the degrees of freedom.
A word of further explanation is in order here.
While the term (n1) is used by the majority of statisticians, it is possible that you might on occa- sion see the term n used as the denominator instead of (n 1) when calculating variance.
The mathematical reasoning behind the state- ment that (n 1) is the better choice is beyond the scope of this encyclopedia’s discussions.
Nonetheless, a simple explanation makes the point.
Whenever a single research study is conducted, a sample of study participants is cho- sen from the population of all individuals who could theoretically have participated as subjects.
The data collected from the subjects who did participate facilitate the precise calculation of the variance in the characteristic of interest to the researchers (reduction in blood pressure, reduction in an assessment of depression, etc.).
However, this precisely calculated value is not of primary interest. What is of most interest is an estimate of the variance that would be seen in the general population of individuals who may be exposed to the intervention of interest if the study reveals that the intervention is both safe and also of therapeutic benefit. That is, the goal is to use statistical methodology to estimate in an optimum manner how well the results of a single experimental study will generalize to the general population of patients should the intervention become widely used. The best estimate of the population variance is generated by the use of (n1) as the degrees of freedom, that is, as the denominator when the sum of squares is divided by the degrees of freedom.
Cross-References
▶Standard deviation
▶Variance
Degrees of Freedom 549
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Dekker, Joost
Joost Dekker
Department of Psychiatry and Department of Rehabilitation Medicine, VU University Medical Centre, Amsterdam, The Netherlands
Biographical Information
Joost Dekker was born in Doetinchem, the Netherlands, on June 23, 1951. He received a BSc in chemistry (Utrecht, 1973, cum laude) and MSc in psychology (Utrecht, 1980). He obtained his PhD in 1988 (Utrecht, cum laude).
He is a licensed health psychologist. He was senior researcher at the WHO Collaborating Cen- ter on Quality of Life in Relation to Health Care, Amsterdam (1987–1988), and senior researcher and subsequently head of the research department at the Netherlands Institute of Primary Health Care, Utrecht (1988–2001). He was also director of the Institute of Health and Welfare Studies, Amsterdam (2001–2007).
Dekker is currently Professor of Allied Health Care at the Department of Psychiatry and the Department of Rehabilitation Medicine, VU University Medical Center, Amsterdam, the Netherlands (1997–present). He is chair of the research track Soma & Psyche in the Mental Health research program, EMGO Institute for Health and Care Research, and leader of the Quality of Life research program, Cancer Center
Amsterdam. He is “dosent” of Psychological Aspects of Rehabilitation at the Faculty of Sports and Health Sciences, University of Jyv€askyl€a, Finland.
Dekker’s research concerns behavioral factors in somatic disease, in the clinical epidemiological tradition. He focuses on musculoskeletal disor- ders, neurological disorders, and – recently – cancer. He has obtained grants from numerous agencies, including the Ministry of Health, Netherlands Organization for Health Research and Development, and NGOs. He is (co)author of more than 225 international peer-reviewed scientific publications, more than 80 national peer-reviewed scientific publications, and more than 90 scientific publications in books, reports, and other journals. He served as editor in chief (2007–2011) and associate editor (1993–2006) of the International Journal of Behavioral Medicine.
He performs editorial services for a wide range of scientific journals and has supervised 21 success- fully defended PhD theses.
Dekker is president elect of the International Society of Behavioral Medicine (2010–2012) and will serve as president from 2012 to 2014.
Other positions in ISBM include member of the Board (2007–present), member of the Governing Council (1994–2006), chair of the Strategic Planning Committee (2004–2006), chair of the Nominations Committee (2006), and co-chair (1996–1998) and chair (1998–2002) of the Education and Training Committee. He is involved in other international and national boards and committees. Examples include the Society of Behavioral Medicine, the Cochrane Collaboration, Netherlands Health Council, Netherlands Health Research Council, Netherlands Behavioral Medicine Federation, and Royal Netherlands Society of Physiotherapy.
He has contributed to the organization of numerous international and national conferences.
Major Accomplishments
Dekker developed the theory on behavioral and neuromuscular factors in activity limitations in
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550 Dekker, Joostosteoarthritis. The theory provides an integrated model of how behavioral factors (negative affect and avoidance of activities) and neuromuscular factors (muscle weakness, poor proprioception, and laxity of joints) interact, resulting in activity limitations in this clinical condition. Empirical support for the theory has been obtained in cross-sectional and longitudinal research (Dekker, Tola, Aufdemkampe, & Winckers, 1993; van der Esch, Steultjens, Knol, Dinant, &
Dekker, 2006; van der Esch et al., 2007;
Steultjens, Dekker, & Bijlsma,2002).This theory was used to develop therapeutic approaches aimed at improved performance of activities in osteoarthritis. Examples include “behavioral graded activity” and “stability training.” These therapeutic approaches have been and are being evaluated in randomized clinical trials, which are providing evidence in support of these approaches (Pisters, Veenhof, Schellevis, de Bakker, & Dekker,2010; Veenhof et al.,2006).
He contributes to the integration of psychol- ogy and rehabilitation (including rehabilitation medicine, physiotherapy, and occupational ther- apy). This integrated approach results in novel theories and innovative treatments. The previ- ously mentioned research on activity limitations in osteoarthritis illustrates the integration of psy- chology and rehabilitation. Other examples include the development of therapeutic approaches for neurological patients, specifically stroke patients with apraxia (Donkervoort, Dekker, Stehman-Saris, & Deelman, 2001;
Donkervoort, Dekker, & Deelman, 2006;
van Heugten et al., 1998) and patients with dementia (Graff et al.,2006).
Dekker also contributes to the scientific foun- dation of rehabilitation medicine, physiotherapy, and occupational therapy. This work concerns the application of the International Classification of Functioning in these disciplines (Dekker,1995), summarizing the evidence in support of exercise therapy in a wide range of disorders (Baar, Assendelft, Dekker, Oostendorp, & Bijlsma, 1999; Smidt et al., 2005), assessing prognostic factors for quality of life (Braamse et al.,2011;
van der Waal, Terwee, van der Windt, Bouter, &
Dekker, 2005), summarizing the evidence in
support of occupational therapy in numerous dis- orders (Steultjens, Dekker, Bouter, Leemrijse, &
van den Ende, 2005), assessing the impact of comorbidity on pain and activity limitations (van Dijk et al., 2010), and contributing to the development of measurement instruments and clinimetrics (Dekker, Dallmeijer, & Lankhorst, 2005).
He strongly supports the implementation of his research into clinical practice. This has resulted in the foundation of an outpatient clinic for advanced rehabilitation in osteoarthritis, the development and implementation of a national consensus on the treatment of osteoarthritis (van den Ende et al.,2010), and the implementa- tion of screening and treatment for psychological distress in patients with multiple sclerosis and cancer.
In the role of editor in chief, Dekker contributed to the definition of the profile of the International Journal of Behavioral Medicine (Dekker, 2007). IJBM has been defined as an interdisciplinary journal, publishing research on factors relevant to health and illness. The scope of IJBM extends from biobehavioral mechanisms, clinical studies on diagnosis, treatment, and reha- bilitation to research on public health, including health promotion and prevention. IJBM is an international journal: manuscripts originate from all over the world, addressing issues related to both local and global health.
Cross-References
▶Arthritis
▶Cancer Survivorship
▶Chronic Pain
▶Evidence-Based Behavioral Medicine (EBBM)
▶Exercise
▶International Society of Behavioral Medicine
▶Neurological
▶Occupational Therapy
▶Physical Therapy
▶Psychometrics
▶Quality of Life: Measurement
▶Rehabilitation
Dekker, Joost 551
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References and Readings
Baar, M. E. V., Assendelft, W. J. J., Dekker, J., Oostendorp, R. A. B., & Bijlsma, J. W. J. (1999).
Effectivenss of exercise therapy in patients with oste- oarthritis of the hip or knee: A systematic review of randomized clinical trials.Arthritis & Rheumatism, 42, 1361–1369.
Braamse, A. M., Gerrits, M. M., van Meijel, B., Visser, O., van Oppen, P., Boenink, A. D. et al (2011). Predictors of health-related quality of life in patients treated with auto- and allo-SCT for hematological malignancies.
Bone Marrow Transplant. doi:10.1038/bmt.2011.130.
Dekker, J. (1995). Application of the ICIDH in survey research on rehabilitation: The emergence of the func- tional diagnosis. Disability and Rehabilitation, 17 (3–4), 195–201.
Dekker, J. (2007). Defining the profile. International Journal of Behavioral Medicine, 14, 1–2.
Dekker, J., Dallmeijer, A. J., & Lankhorst, G. J. (2005).
Clinimetrics in rehabilitation medicine: Current issues in developing and applying measurement instruments 1.
Journal of Rehabilitation Medicine, 37(4), 193–201.
Dekker, J., Tola, P., Aufdemkampe, G., & Winckers, M.
(1993). Negative affect, pain and disability in osteoar- thritis patients: The mediating role of muscle weak- ness.Behavior Research and Therapy, 31, 203–206.
Donkervoort, M., Dekker, J., & Deelman, B. (2006). The course of apraxia and ADL functioning in left hemi- sphere stroke patients treated in rehabilitation centres and nursing homes. Clinical Rehabilitation, 20(12), 1085–1093.
Donkervoort, M., Dekker, J., Stehman-Saris, F. C., &
Deelman, B. G. (2001). Efficacy of strategy training in left hemisphere stroke patients with apraxia:
A randomised clinical trial.Neuropsychological Reha- bilitation, 11, 549–566.
Graff, M. J., Vernooij-Dassen, M. J., Thijssen, M., Dekker, J., Hoefnagels, W. H., & Rikkert, M. G.
(2006). Community based occupational therapy for patients with dementia and their care givers:
Randomised controlled trial.British Medical Journal, 333(7580), 1196.
Pisters, M. F., Veenhof, C., Schellevis, F. G., de Bakker, D. H., & Dekker, J. (2010). Long-term effectiveness of exercise therapy in patients with oste- oarthritis of the hip or knee: A randomized controlled trial comparing two different physical therapy inter- ventions. Osteoarthritis and Cartilage, 18(8), 1019–1026.
Smidt, N., de Vet, H. C., Bouter, L. M., Dekker, J., Arendzen, J. H., de Bie, R. A., et al. (2005). Effective- ness of exercise therapy: A best-evidence summary of systematic reviews.The Australian Journal of Physio- therapy, 51(2), 71–85.
Steultjens, M. P., Dekker, J., & Bijlsma, J. W. (2002).
Avoidance of activity and disability in patients with osteoarthritis of the knee: The mediating role of muscle strength.Arthritis and Rheumatism, 46(7), 1784–1788.
Steultjens, E. M., Dekker, J., Bouter, L. M., Leemrijse, C. J., & van den Ende, C. H. (2005). Evi- dence of the efficacy of occupational therapy in differ- ent conditions: An overview of systematic reviews.
Clinical Rehabilitation, 19(3), 247–254.
van den Ende, C. M., Bierma-Zeinstra, S. M., Vlieland, T. P., Swierstra, B. A., Voorn, T. B., &
Dekker, J. (2010). Conservative treatment of hip and knee osteoarthritis: A systematic, step-by-step treatment strategy. Nederlands Tijdschrift voor Geneeskunde, 154, A1574.
Van der Esch, M., Steultjens, M., Harlaar, J., Knol, D., Lems, W., & Dekker, J. (2007). Joint proprioception, muscle strength, and functional ability in patients with osteoarthritis of the knee.Arthritis and Rheumatism, 57(5), 787–793.
van der Esch, M., Steultjens, M., Knol, D. L., Dinant, H., & Dekker, J. (2006). Joint laxity and the relationship between muscle strength and functional ability in patients with osteoarthritis of the knee.
Arthritis and Rheumatism, 55(6), 953–959.
van der Waal, J. M., Terwee, C. B., van der Windt, D. A., Bouter, L. M., & Dekker, J. (2005). The impact of non- traumatic hip and knee disorders on health-related quality of life as measured with the SF-36 or SF-12.
A systematic review.Quality of Life Research, 14(4), 1141–1155.
van Dijk, G. M., Veenhof, C., Spreeuwenberg, P., Coene, N., Burger, B. J., van Schaardenburg, D., van den Ende, C. H., Lankhorst, G. J., Dekker, J. (2010). CARPA Study Group. Prognosis of limitations in activities in osteoarthritis of the hip or knee: a 3-year cohort study.
Archives of Physical Medicine and Rehabilitation, 91:58–66.
van Heugten, C. M., Dekker, J., Deelman, B. G., van Dijk, A. J., Stehmann-Saris, J. C., & Kinebanian, A.
(1998). Outcome of strategy training in stroke patients with apraxia: A phase II study.Clinical Rehabilitation, 12(4), 294–303.
Veenhof, C., Koke, A. J., Dekker, J., Oostendorp, R. A., Bijlsma, J. W., van Tulder, M. W., et al. (2006). Effec- tiveness of behavioral graded activity in patients with osteoarthritis of the hip and/or knee: A randomized clinical trial.Arthritis and Rheumatism, 55(6), 925–934.
Delay Discounting
▶Impulsivity
Deliberate Self-Harm
▶Suicide
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552 Delay DiscountingDelta Sleep
▶Slow-Wave Sleep
Dementia
Bonnie Levin
Department of Neurology, University of Miami Medical Center, Miami, FL, USA
Synonyms
Cognitive impairment; Cortical dementia;
Dementing illness
Definition
Dementia is a disorder characterized by a progressive decline in intellectual function or behavior severe enough to cause impairment in social and occupational functioning.
Description
The term dementia is derived from the Latin words de (“without”) and mens (“the mind”).
The most widely used criterion for diagnosing dementia is the DSM-IV, which defines dementia as a disorder characterized by progressive decline in intellectual function or behavior severe enough to cause impairment in social and occupational functioning. Memory loss is the hallmark feature as well as impairment in one or more cognitive abilities, including language, reasoning, execu- tive function, praxis, and visuospatial skills.
The DSM-V, which is expected to be published in 2012, has adopted the term
“Neurocognitive Disorders” and further subdivided it into “Major” and “Minor” to replace the DSM-IV classification of “Delirium, Dementia, and Amnestic and Other Cognitive Disorders.”
There are four dementia syndromes that account for approximately 90% of cases. They are Alzheimer’s disease, vascular dementia, dementia with Lewy bodies, and frontotemporal dementia.
Alzheimer’s disease: Alzheimer’s disease (AD) is the most common dementia accounting for 50% of all cases. The major pathology is an abnormal extracellular accumulation of beta- amyloid peptide and intracellular accumulation of tau protein. Beta-amyloid is believed to be the main component of senile plaques (SPs) and tau is involved in the development of neurofibrillary tangles (NFT). Neuropathological examination of AD brains reveals that most cases of AD have a combination of NFT and SP. The NFTs initially appear in the hippocampus and entorhi- nal cortex and then extend to the neocortex. SPs tend to be seen more in the association cortex.
Memory changes have been correlated with hip- pocampal and entorhinal pathology whereas more global cognitive decline is seen with neo- cortical involvement. AD onset is typically insid- ious, often taking years before the correct diagnosis is made. The first clinical criteria based on consensus were published in l983, referred to as the NINCDS-ADRDA. The advancement in MR imaging, PET imaging, CSF assays, and other biomarkers have shown that the older criteria are no longer well suited to diagnose AD and newer guidelines for all- cause dementia and AD dementia, which is fur- ther subdivided into amnestic and non-amnestic presentations, have recently been published (Dubois et al.,2007).
Cardinal features of the disease are progres- sive decline in mental status functions, including memory loss, and one or more cognitive impair- ments involving language, executive, visuospa- tial/perceptual dysfunction, apraxia, and agnosia.
The cognitive deficits seen in AD are progressive and interfere with activities of daily living (ADL). The average time course for AD is between 8 and 12 years after diagnosis, but it can last as long as 20. It is now accepted that there is a prodromal phase in which individuals exhibit mild cognitive impairment, also referred to as MCI, before reaching the threshold for early dementia (Peterson,2000).
Dementia 553
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There are three stages of AD. In mild AD, individuals typically present with problems recalling recent events with relative sparing of older memories. Other frequent cognitive prob- lems include difficulty in solving problems and carrying out complex multi-step tasks, making sound decisions, planning difficulties, and prob- lems in holding information in mind. Changes in personality are also common, with irritability and apathy among the most frequent complaints voiced by caregivers. Individuals in the early stages of AD may also exhibit empty speech, problems finding words, and have difficulty expressing their ideas. In the midstage or moder- ate AD, individuals become more confused and their memory loss is more pervasive. They may have difficulty retrieving older memories such as their address, school they attended, or names of relatives. Assistance with basic ADLs such as grooming, toileting, and other self-care activities may be necessary. Personality changes are more pervasive and it is not unusual for caregivers to report aggression and paranoia. In the late or severe stage of AD, afflicted individuals have lost the ability to communicate beyond occa- sional words or phrases and require full time assistance for all self-care activities. At this stage, motor symptoms are common as well as loss of bowel, bladder, and swallowing abilities.
Most AD patients die of complications of chronic illness (pneumonia).
Vascular dementia: It is estimated that nearly two thirds of individuals who experience a stroke will have some degree of cognitive impairment, with roughly a third exhibiting frank dementia (Selnes & Vinters,2006). Cognitive impairment resulting from vascular factors has been termed,
“vascular cognitive impairment” or VCI. Various components of the “metabolic syndrome,” a term that refers to a cluster of cardiovascular risk fac- tors, including diabetes, hypertension, hyperlip- idemia, hypertriglycemia, and impaired glucose tolerance, have been linked to age-related cogni- tive decline. Postmortem studies have revealed that VCI can also coexist with AD pathology, and those with both pathologies show a greater degree of cognitive impairment (REF). Since many of the vascular risk factors can be modified
following changes in one’s lifestyle (diet, exer- cise, not smoking, etc.) and medication, it may be possible to improve or even decrease the inci- dence of VCI with the appropriate intervention (Gorelick et al.,2011).
Dementia with Lewy bodies: Dementia with Lewy bodies (DLB), also known as Lewy body dementia, Lewy body disease, and cortical Lewy body disease, is the second most common demen- tia after Alzheimer’s disease. DLB can present as a movement disorder resembling Parkinson’s dis- ease with cognitive changes or with memory and dysexecutive changes suggestive of Alzheimer’s disease with visual hallucinations and/or delu- sions. Other presenting features of DLB include fluctuating levels of attention, characterized by drowsiness, starring off, lethargy, a history of falling, sleep-related disturbances, and auto- nomic dysregulation involving body temperature, blood pressure, urinary difficulties, constipation, and swallowing difficulties. Risk factors are age (>60 years), gender (male), and family history.
Frontal temporal dementia: Frontal temporal dementia (FTD) is a category of conditions involving atrophy and neuronal loss of the frontal and temporal lobes, resulting in prominent lan- guage impairment and behavioral decline. It is the most prevalent dementia among younger indi- viduals. It is estimated that between 20% and 50% of individuals with dementia under 65 years of age have FTD (REF). Three FTD syndromes have been proposed: behavioral vari- ant, semantic dementia, and progressive nonfluent aphasia. In the behavioral variant, neu- ropsychiatric features, characterized by emo- tional dysregulation, are prominent early in the disease. Social inappropriateness, lack of insight, apathy, disinhibition, and diminished activity are frequent as well as more extreme behaviors including poor hygiene, hyperorality, shoplifting, and other impulse control problems. This variant is often misdiagnosed as depression due to the apathetic behavioral style. Frank psychosis is unusual but seen most often among individuals with Alzheimer’s disease (Cardarelli, Kertesz, &
Knebl, 2010; Neary et al., 1998). In semantic dementia, patients present with fluent speech that is devoid of meaning and may contain
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554 Dementiasemantic paraphasias. The central feature is lan- guage output characterized by the use of words that approximate the intended word, such as
“thing to eat with” for knife or “clothes” for skirt. In addition, this variant is also associated with associative agnosia, or the inability to rec- ognize and assign meaning to objects and facial recognition deficits, including well-known figures such as celebrities (Cardarelli et al., 2010; Neary et al.,1998). The third variant, pro- gressive nonfluent aphasia, is characterized by speech that is agrammatical, nonfluent, stuttering or halting, and effortful. Word retrieval difficul- ties or frank anomia are common with phonemic paraphasias such as saying “dat” for cat or
“drother” for mother. Other impairments include difficulties with comprehension, reading, and repetition. Median survival
