Please see attachment
Case Example – Emily*
“Only upon the repeated and fervent insistence of her parents did 19-year-old Emily reluctantly agree to see a psychiatrist. “It’s not me you want to see,” Emily proclaimed emphatically. “It’s my insane parents who need your help.” Emily did not offer a chief complaint, aside from the concern that her parents were driving her “crazy.” She added, “Everything is going great in my life. I have plenty of friends, go out almost every night, and always have lots of fun.”
While Emily was taking some time away from “the so-called real wired,” her sister was attending Duke University, her younger brother was excelling at a competitive private high school, and both her parents seemed to enjoy their careers as radiologists. She asked, “Don’t you think that’s enough strivers for one family?”
Emily agreed to have her parents join the session, and they told a different story. They tearfully disclosed that their daughter had become irritable, unproductive, and oppositional. She drank to intoxication almost every night, often not returning home for an entire weekend. In searching her room, they had found small amounts of marijuana, alprazolam (Xanax), cocaine, and prescription stimulants. The parents described the changes in Emily’s personality as “an adolescent nightmare” and described her friends as “losers who do nothing but dye their hair, get tattoos, and hate everything.” Emily’s attitudes and behavior contrasted markedly with those of her parents and siblings. “We don’t mind that she is doing her own thing and that she isn’t conservative like the rest of us,” her father said, “but it’s like we don’t even recognize who she’s become.”
According to her parents, Emily’s “adolescent nightmare” began 4 years earlier. She had apparently been a studious 15-year-old girl with a lively sense of humor and a wide circle of “terrific friends.” “Almost overnight,” she began to shun her longtime friends in favor of “dropouts and malcontents” and began to accumulate traffic tickets and school detentions. Instead of her former brightened curiosity, Emily manifested a lack of interest in all her academic subjects, and her grades dropped form As to Ds. The parents were at an absolute loss to explain the sudden and dramatic change.
The abrupt change in performance led the psychiatrist to ask Emily to take a battery of neuropsychological tests so the results could be compared with those of test she had taken when she had applied to a private high school several years earlier. In particular, Emily retook two high school admissions tests: the System for Assessment and Group Evaluation (SAGE), which measures a broad array of academic and perceptual aptitudes, and Differential Aptitude Tests (DAT), which focus on reasoning, spelling, and perceptual skills.
On the SAGE, her average percentile scores dropped from the upper 10% for a 13 -year-old to the bottom 10% for an adult (and the bottom 20% for a 13-year-old). When Emily took the DAT at age 13, she scored in the highest range for ninth graders across almost all measures. Her worst result had been in spelling, where she scored at the second-highest level. Upon repeating the test at age 19, she scored below the high school average in all measures.
EEG, brain CT, and T2-weighted brain MRI images did not show evidence of structural brain damage, However, fluid-attenuated inversion recovery (FLAIR) T2-weighted MRI displayed a clear lesion in the left frontal cortex, highly suggestive of previous injury to that region.
Upon further questioning about the crucial period in which she seemed to have changed, Emily admitted to being in a traffic accident with her now ex-boyfriend, Mark. Although Emily did not recall much from this episode, she remembered that she hit her head and that she had bad headaches for many weeks thereafter. Because Emily was not bleeding and there was no damage to the car, neither Mark nor Emily reported the incident to anyone. With Emily’s permission, the psychiatrist contacted Mark, who was away at college but a willing and excellent historian. He remembered the incident well. “Emily hit her head very, very hard on the dashboard of my car. She was not totally unconscious but very dazed. For almost 3 hours, she spoke very slowly, complained that her head hurt badly, and was confused. For about 2 hours she didn’t know where she was, what day it was, and when she had to get home. She also threw up twice. I was really scared, but Emily didn’t want me to worry her parents since they’re so overprotective And then she broke up with me, and we’ve hardly spoken since.”
*From DSM 5 Clinical Cases, Barnhill, J. (Ed.), 2014.
No more than 2 pages; APA format and scholarly sources
Assignment will be submitted through safe assign
You want your case to be well organized and well written to be sure that information you include is easily identified and followed by your reader. The following can be used as section headings to help you organize your paper:
·
Brief overview of relevant symptoms from case
· Diagnosis 1
· Reasoning/evidence
· Diagnosis 2
· Reasoning/evidence
· Diagnosis 3
· Reasoning/evidence
Brief overview of relevant symptoms from case
· Please see case study attachment
List Diagnosis 1: (ICD & DSM diagnoses)
· Problems related to education and literacy
Diagnosis 1 Reasoning/Evidence
· She lacked interest in her academics and scored low in her grades; also scored low on the test the psychiatrist had given her
List Diagnosis 2: (ICD & DSM diagnoses)
· Problems related to unbringing
Diagnosis 2 Reasoning/Evidence
· Parents were overprotected; she hid the accident from her parents
· She didn’t want to live up to her parents expectations
List Diagnosis 3: (if any)
· Procedure and treatment not carried out, unspecified reason
Diagnosis 3 Reasoning/Evidence
-she refused to get treatment to her head when she was in the accident with her ex boyfriend because she didn’t want to worry her parents
There are 2 assignments: assignments will be submitting for plagiarism
Assignment 1: see attachment for chapter 12 textbook content and videos
1. Prepare a PAPER (APA style) , no more or less than 3 pages (in addition to a cover page and a reference page) of text, on the topic of neuro-cognitive disorders, specifically traumatic brain injury (a sudden onset) or age/disease related neuro-cognitive disorder (develops over time) in either child/adolescent clients or adult clients. Don’t forget to cite and source in the text of your paper!
Focus on and be sure to include information on the following:
a. how a neuro-cognitive disorder might manifest in your chosen “client” (child/teen or adult)
b. how the neuro-cognitive disorder is likely to impact the overall functioning of the “client” on a daily basis (socially, emotionally, environmentally, within the family etc.)
c. one thing you think would be most important in your developing a counseling relationship with your “client”
Please see attachment for assignment 2 (Emily case study)
Youtube videos:
Understanding Neurodevelopmental Disorders and Autism
neurocognitive disorder/dementia
Textbook:
Sue, D., Sue, D. W., Sue, D., & Sue, S. (2014). Essentials of understanding abnormal behavior (2nd ed.). Belmont, CA: Wadsworth Cengage Learning.
Chapter 12
Although DSM-5 defines only three major categories of neurocognitive disorders (major neurocognitive disorder, mild neurocognitive disorder, and delirium), the classification system recognizes that the symptoms of these disorders result from many disease processes or medical conditions. Therefore, medical assessment and determining specific etiology are important components of the diagnostic process. Thus, before we present the DSM-5 neurocognitive disorder categories, we discuss an important first step—assessing and documenting a person’s brain function and adaptive, day-to-day mental functioning.
Medical professionals and medical procedures play a key role in assessing and diagnosing neurocognitive disorders (Blaze, 2013). Physicians sometimes evaluate patients for brain damage during hospitalization following a traumatic event. Additionally, physicians often initiate assessment when an individual or family member is concerned about declining memory or other changes in mental functioning.
Clinicians begin by gathering background information, paying particular attention to mental changes involving memory, thinking, or self-help skills. They carefully evaluate overall mental functioning, personality characteristics, and coping skills, as well as behaviors and emotional reactivity. They rule out sensory conditions (such as impaired hearing or vision) or emotional factors such as depression as the primary cause of the cognitive decline. Assessment frequently involves screening of mental status, including memory and attentional skills and orientation to time and place. Additionally, psychologists may perform more extensive neuropsychological testing to pinpoint areas of cognitive difficulty or to evaluate emotional functioning. The goal is to see how a person’s cognitive skills and adaptive behavior compare with others of the same gender, age range, and educational level.
Chronic Traumatic Encephalopathy and Suicide
An autopsy of Junior Seau, a former NFL linebacker who committed suicide in May 2012, revealed that he suffered from chronic traumatic encephalopathy, a condition resulting from recurrent head trauma that can lead to depression and cognitive difficulties. Autopsies on other NFL players who committed suicide have revealed similar brain pathology.
Margaret Bowles/SCG/ZUMAPRESS. com/Alamy
Medical tests help medical professionals rule out easily treatable physical causes for the symptoms. In some cases, something as simple as a urinary tract infection can impair cognitive functioning. Similarly, blood tests can detect treatable medical conditions such as impaired thyroid or liver functioning or low levels of vitamin B12. Neurological testing procedures discussed in
Chapter 3
, such as electroencephalograph (EEG), computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography (PET), are sometimes used to assess current brain functioning, as well as to monitor progression of
brain pathology
. Physicians decide which tests to use based on the person’s specific symptoms, as well as the risks and benefits of the procedures.
Did You Know?
Due to an aging population and lifestyle factors that affect brain health, it is estimated that the number of people affected by dementia worldwide will nearly double every 20 years—increasing from 35.6 million in 2010 to 115.4 million in 2050.
Source: Prince et al., 2011
After reviewing all of the data from medical and psychological tests, the professionals involved have a much better understanding of probable causes of the impairment. Neuropsychological testing and standardized cognitive screening also provide objective information about the severity of cognitive difficulties. Comprehensive baseline assessments are used to objectively monitor progress or decline in functioning. Although neuropsychological and neurological tests can assist with diagnosis, they provide limited information regarding prognosis or course of the disorder (Karceski, 2013). Even when there is no cure for a condition, early diagnosis may provide an opportunity for interventions that delay the progression of a condition or allow the individual to make decisions about future care needs before symptoms worsen.
We will now review the three major categories of neurocognitive disorders described in DSM-5: (a) major neurocognitive disorder, (b) mild neurocognitive disorder, and (c) delirium (see
Table 12.1
).
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Table 12.1
Neurocognitive Disorders
Disorder
DSM-5 Criteria
Major neurocognitive disorder
Significant decline in performance in one or more cognitive areas; the deficits are severe enough to interfere with independence
Mild neurocognitive disorder
Moderate decline in performance in one or more cognitive areas; compensatory strategies may be required to maintain independence
Delirium
Sudden changes in cognition, including diminished awareness and impaired attention and focus
Source: Based on information from APA (2013).
Case Study
Ms. B., an 80-year-old woman, became increasingly agitated, screaming, spitting, striking staff. . . . Her speech was loud, disarticulate. . . . She repeatedly yelled “get out.” Ms. B. had recently moved to an assisted-living facility due to her declining language, social, and self-care skills (Bang, Price, Prentice, & Campbell, 2009, p. 379).
Individuals diagnosed with
major neurocognitive disorder
show significant decline in both of the following:
· one or more areas of cognitive functioning, involving attention and focus, decision making and judgment, language, learning and memory, visual perception, or social understanding (
Table 12.2
); and
· the ability to independently meet the demands of daily living (this can involve more complex skills such as managing bills or medications).
Table 12.2
|
Cognitive Domain |
Skills Affected |
|
Complex attention |
Focus, planning, working memory |
|
Executive ability |
Decision making, mental flexibility |
|
Learning and memory |
Long-term and recent memory; ability to learn new tasks |
|
Language |
Understanding and use of language |
|
Visual-perceptual ability |
Construction, visual perception |
|
Social cognition |
Recognition of emotions, understanding of social situations, behavioral self-control |
Source: APA (2013).
The evidence from cognitive screening, neuropsychological testing, and interviews with the individual and others knowledgeable about the person’s functioning must confirm that the person is demonstrating a significant skill deficit that represents a decline from prior levels of functioning. When known, clinicians specify the underlying medical circumstances causing the disorder. In the case of Ms. B., screening tests and input from her family members and caregivers revealed significant impairment involving declines in many areas of functioning. Although diagnosis of major neurocognitive disorder requires a significant deficit in only one cognitive area, deficits in multiple areas are common.
Did You Know?
Veterans diagnosed with post- traumatic stress disorder (PTSD) have a greater risk for dementia compared to other veterans, including veterans who received traumatic wartime injuries. It is unclear if PTSD is a risk factor for dementia or if another factor increases risk of both disorders.
Source: Qureshi et al., 2010
Dementia
is the decline in mental functioning and self-help skills that result from a major neurocognitive disorder. People with dementia may forget the names of significant others or past events. They may also display difficulties with problem solving and impulse control. Agitation due to confusion or frustration is also common (Morris, 2012). Dementia typically has a gradual onset followed by continuing cognitive decline. Age is the most studied and the strongest risk factor for dementia. The longer a person lives, the greater the chance of developing dementia. In the United States, approximately 15 percent of individuals over age 70 have dementia (Hurd, Martorell, Delavande, Mullen, & Langa, 2013). Because women have a longer life span than men, they are more likely to develop dementia.
Individuals diagnosed with
mild neurocognitive disorder
demonstrate a modest decline in at least one major cognitive area (see
Table 12.2
). The degree of cognitive impairment is more subtle than that seen in major neurocognitive disorder. Individuals with a mild neurocognitive disorder are often able to participate in their normal activities, although they may require extra time or effort to complete complex tasks. Although accommodations to maintain independence may be required (e.g., hiring someone to manage finances), overall independent functioning is not compromised.
Mild neurocognitive disorder is often an intermediate stage between normal aging and major neurocognitive disorder or dementia. One of the major challenges in diagnosing mild neurocognitive disorder is ensuring that the symptoms are, in fact, a disorder and not the effects of physical or emotional difficulties associated with aging (Blaze, 2013). The cognitive slowing and occasional memory lapses associated with normal aging have less of an effect on daily functioning compared to the declines associated with mild or major neurocognitive disorder (see comparisons in
Table 12.3
).
Table 12.3
|
Normal Aging |
Neurocognitive Disorder |
|
Is independent in most activities, but may need occasional assistance with electronic devices, etc. |
Has difficulty or requires assistance with normal, day-to-day activities |
|
Occasionally misplaces things and locates them after searching |
Places items in unusual locations; may not recall objects are missing or may accuse others of stealing |
|
Occasionally forgets a name, word, or appointment |
Frequently forgets words or recently learned information; uses incorrect words; repeats the same questions or comments |
|
Is slower to complete mental or physical activities |
Has difficulty performing familiar tasks |
|
Shows concern about occasional forgetfulness |
Is unaware or unconcerned about memory difficulties |
|
Experiences occasional distractibility |
Exercises poor judgment; fails to remember important dates or details |
|
Continues interacting socially; occasionally feels tired |
Exhibits decreasing social skills, declining social interest, and passivity; difficulty following or contributing to conversations |
|
Occasionally gets lost |
Experiences increasing disorientation and confusion; becomes lost or unaware of present location |
|
Undergoes normal changes in mood |
Has personality changes or drastic mood shifts; may seem apathetic, anxious, confused, or depressed |
© Cengage Learning®
The primary distinction between major and mild neurocognitive disorder is the severity of the decline in cognitive and independent functioning (Blaze, 2013). In fact, mild and major neurocognitive disorders are sometimes earlier and later stages of the same disease process. For example, someone in the early stages of a progressive disorder such as
Alzheimer’s disease
may initially remain independent and display only moderate changes in cognitive functioning. As the disease progresses, however, the symptoms increase in severity and begin to affect independent functioning. Unfortunately, the mild cognitive impairment associated with early dementia often goes undiagnosed; when this occurs, those affected do not have the benefit of receiving practical information about the condition or the opportunity to plan for future care before experiencing more severe cognitive difficulties (Prince, Bryce, & Ferri, 2011).
Did You Know?
In a simulated driving experiment, individuals with dementia received more speeding tickets, ran more stop signs, and were involved in more accidents than similar individuals without dementia.
Source: de Simone, Kaplan, Patronas, Wassermann, & Grafman, 2006
In some situations, a diagnosis is upgraded from major to mild neurocognitive disorder; this might occur following partial recovery from a stroke or traumatic brain injury. In some cases, early diagnosis and treatment of nondegenerative conditions can result in a return to normal functioning (R. C. Petersen, 2011). Unfortunately, individuals with either major or mild neurocognitive disorder can show an abrupt decline in functioning if they experience an episode of delirium, the third type of neurocognitive disorder.
Case Study
Police brought an 18-year-old high school senior to the emergency department after he was picked up wandering in traffic. He was angry, agitated, and aggressive. In a rambling, disjointed manner he explained that he had been using “speed.” In the emergency room he had difficulty focusing his attention, frequently needed questions repeated, and was disoriented as to time and place (Spitzer, Gibbon, Skodol, Williams, & First, 1994, p. 162).
Delirium
is an acute state of confusion characterized by disorientation and impaired attentional skills. This disturbance in a person’s mental abilities results from physiological factors such as alcohol or drug intoxication or exposure to toxins (APA, 2013). Delirium can emerge in the context of a major or mild neurocognitive disorder, but it often appears independently as seen in the case of the teenager using drugs. Delirium differs from mild and major neurocognitive disorder based on its core characteristics (disturbance in awareness and difficulty focusing, maintaining, or shifting attention), as well as its abrupt onset and fluctuating course. Delirium typically develops over a period of several hours or days. Symptoms can be mild or quite severe, and can be brief or last for several months. People experiencing delirium often have significant cognitive difficulties, including confusion regarding where they are or the time of day. Wandering attention, disorganized thinking, and rambling, irrelevant, or incoherent speech may be present. Psychotic symptoms such as delusions or hallucinations may also occur. Symptoms of delirium fluctuate and can range from agitation and combativeness to drowsy, unresponsive behavior.
Hospital Delirium
Delirium is frequently experienced by individuals who are hospitalized, especially among those who are seriously ill and receiving intensive care.
Craig F. Walker/Denver Post/Getty Images
Because delirium is caused by relatively sudden neurological dysfunction (Choi et al., 2012), treatment involves identifying the underlying cause. Possible causes include high fever; severe dehydration or malnutrition; acute infection; sensitivity to a medication or combination of medications; alcohol, drug, or inhalant intoxication; physiological withdrawal from alcohol, sedatives, or sleeping medications; or brain changes associated with a neurocognitive disorder. Additionally, when people are ill or elderly, they are more likely to develop delirium with medical illness, severe stress, or surgical procedures. Given the multiple stressors experienced during hospitalization (illness, sleep deprivation, recovery from surgery and anesthetics), episodes of hospital-associated delirium are common, especially among older adults. Delirium associated with hospitalization is illustrated in the following case study.
Case Study
Justin Kaplan, an alert 84-year-old Pulitzer Prize–winning historian hospitalized after contracting pneumonia, describes an episode of delirium in which he fought with aliens: “Thousands of tiny little creatures, some on horseback, waving arms, carrying weapons like some grand Renaissance battle.” In an attempt to “attack the aliens,” Kaplan fell out of bed, injuring himself. He later threatened to kill his wife and kicked a nurse who was trying to restrain him. Once his medical condition improved, the delirium subsided (Belluck, 2010).
As you can see from the case of Mr. Kaplan, the severe symptoms of hospital delirium can distress loved ones, especially because there is usually no prior history of such behavior. Hospital delirium is more common in older individuals and can result in longer hospital stays, lower rates of survival, and persistent cognitive impairment (Patel, Poston, Pohlman, Hall, & Kress, 2014). Fortunately, many hospitals attempt to detect and intervene with delirium in its earliest stages to prevent these consequences.
Checkpoint Review
1. Why is careful assessment important when diagnosing neurocognitive disorders?
2. Compare and contrast major neurocognitive disorder, mild neurocognitive disorder, and delirium.
Etiology of Neurocognitive Disorders
Amnestic Disorder: Mike
Mike talks about his struggles with amnestic disorder.
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Neurocognitive disorders result from a variety of medical conditions. Therefore, rather than an etiological discussion using our multipath model, we focus on some of the sources of neurocognitive disorders. We do this because, in most cases, neurocognitive disorders involve an identified or suspected medical condition or disease process. As you will see, some neurocognitive disorders involve neurodegenerative conditions in which symptoms become worse over time (
Table 12.4
) whereas others specific events such as stroke or head injury (
Table 12.5
).
Neurodegeneration
refers to progressive brain damage due to neurochemical abnormalities and the death of brain cells. In contrast with the recovery that is possible in cases of stroke, traumatic brain injury, or substance abuse, individuals with neurodegenerative disorders such as Alzheimer’s disease show decline in function rather than improvement. Neurodegenerative disorders vary greatly in terms of age of onset, skills affected, and course of the disorder.
Table 12.4
|
Etiology |
Characteristics |
||
| Alzheimer’s disease |
Declining cognitive functioning, including early, prominent memory impairment |
||
|
Dementia with Lewy bodies |
Visual hallucinations, fluctuating cognitive impairment, dysfunction in motor skills |
||
|
Parkinson’s disease |
Tremor, muscle rigidity, slow movement, and possible cognitive decline |
||
|
Huntington’s disease |
Involuntary movement, cognitive decline, and emotional instability |
||
|
Frontotemporal lobar degeneration |
Brain degeneration in frontal or temporal lobes that affects language and behavior |
||
|
AIDS dementia complex |
Cognitive decline due to HIV or AIDS |
© Cengage Learning®
Table 12.5
|
Ischemic stroke |
Blockage of blood flow in the brain |
|
Hemorrhagic stroke |
Bleeding within the brain |
|
Traumatic brain injury |
Head wound or trauma |
|
Substance abuse |
Results from oxygen deprivation or other factors associated with intoxication, withdrawal, or chronic substance use |
© Cengage Learning®
As we discuss the various medical conditions associated with neurocognitive disorders, it is important to remember that even with the same underlying brain condition, a variety of factors can influence outcome. For example, people with similar brain trauma may recover quite differently, depending on their personalities, their coping skills, and the availability of resources such as rehabilitation and family support. Additionally, the disruptions in brain function seen in neurocognitive disorders can lead to a variety of behavioral and emotional changes; factors such as apathy, depression, anxiety, or difficulty with impulse control can significantly affect recovery (H. J. Rosen & Levenson, 2009).
Furthermore, insensitivity or impatience toward people with neurocognitive disorders can add to their stress and negatively affect their functioning. Indeed, stress can exacerbate symptoms that stem from the brain pathology itself. From the perspective of our multipath model, the specific brain pathology is the primary biological factor for each condition; however, psychological, social, and sociocultural factors can interact with the neurological condition to affect outcome, as shown in
Figure 12.1
. We now begin our discussion of medical conditions that can result in a neurocognitive disorder.
Figure 12.1Multipath Model of Neurocognitive Disorders
The dimensions interact with specific brain pathology to produce the symptoms and pattern of recovery seen in various neurocognitive disorders.
© Cengage Learning®
Case Study
United States representative Gabrielle Giffords, age 40, was shot in the head on January 8, 2011. The bullet entered into and exited from the left side of her brain. Following surgery, Representative Giffords remained in a
medically induced coma
, a state of deep sedation that allows time for the brain to heal. Part of her skull was removed to accommodate the anticipated swelling of her brain and to prevent further damage. Giffords’ purposeful movements and responsiveness to simple commands were early, encouraging signs. Although extensive therapy helped Giffords regain many language and motor skills, 1 year after the shooting she officially resigned her congressional seat, recognizing that she needed to continue to participate in specialized cognitive and physical rehabilitation in order to maximize her recovery.
Case Study
At age 53, H. N. sustained multiple injuries, including mild bleeding in the brain, when he was hit by a car. Although his initial delirium subsided, other behavioral changes, including pervasive apathy punctuated by angry outbursts, persisted for months. Subsequent MRI scans revealed damage in the orbitofrontal cortex, an area of the brain involved in emotion and decision making (adapted from Namiki et al., 2008, p. 475).
Case Study
P. J. M., a 38-year-old woman, remained in a coma for several weeks after a bicycle accident. After regaining consciousness, she had severe short- and long-term memory deficits (including no recall of the year before her accident) and difficulty using the right side of her body. Despite some improvement, P. J. M. remains unable to drive or return to her work as a university professor (adapted from Rathbone, Moulin, & Conway, 2009, pp. 407–408).
Traumatic brain injury (TBI)
can result from a bump, jolt, blow, or physical wound to the head. As you can see from the cases presented, the degree of impairment and course of recovery associated with a neurocognitive disorder due to TBI can vary significantly. Each year in the United States, approximately 1.7 million people receive emergency room care for head injury; TBI occurs most frequently in young children, older adolescents, and older adults. Approximately 2 percent of the population has a disability related to TBI (APA, 2013). Additionally, head injury contributes to almost one third of injury-related deaths (Faul, Xu, Wald, & Coronado, 2010). Falls, vehicle accidents, and striking or being struck by objects are the leading causes of TBI (
Figure 12.2
).
Figure 12.2Leading Causes of Traumatic Brain Injury
* These data do not include injuries that occurred during military deployment.
Source: Faul, Xu, Wald, & Coronado (2010).
A neurocognitive disorder due to TBI is diagnosed when there is persisting cognitive impairment due to a brain injury; additionally, diagnosis requires that the person experienced loss of consciousness, amnesia, disorientation, or confusion following the event or received neurological testing that documented brain dysfunction (APA, 2013). The effects of TBI can be temporary or permanent and can result in mild to severe cognitive impairment. You have probably heard stories about people who have made a remarkable recovery following TBI. For example, the much-publicized progress of Gabrielle Giffords after her injury illustrates the capacity for brain recovery. In her case, immediate intervention, an excellent rehabilitation program, personal resilience, and social support all played a key role in her progress.
Recovery from Traumatic Brain Injury
Gabrielle Giffords, a former U. S. Congress member, sustained a brain injury from a gunshot in 2011. Here Giffords waves to the delegates at the 2012 Democratic National Convention where she captivated the audience by reciting the Pledge of Allegiance in a halting but strong voice while holding her right hand over her heart with the help of her stronger left hand.
Jeff Siner/MCT/Newscom
Similar conditions facilitated the recovery of news anchor Bob Woodruff, who sustained a life-threatening brain injury resulting from a roadside bomb explosion while he was covering the war in Iraq. After surgery, he spent 36 days in a medically induced coma. He underwent extensive rehabilitation and has since returned to work. In both cases, prompt medical attention and surgery played an important role in survival and recovery.
Did You Know?
Individuals given a simulated driving test after a mild TBI demonstrated reduced response time and diminished hazard perception, which suggests driving immediately after sustaining a TBI may be hazardous.
Source: Preece, Horswill, & Geffen, 2010
As seen in the case studies, the severity, duration, and symptoms of TBI can vary significantly depending on the extent and location of the brain damage, as well as the person’s age. Symptoms can include headaches, disorientation, confusion, memory loss, deficits in attention, poor concentration, fatigue, and irritability, as well as emotional and behavioral changes. Generally, the greater the damage to brain tissue or cells, the more impaired the functioning.
Acute head injuries include concussions, contusions, and cerebral lacerations.
Concussion
, the most common form of traumatic brain injury, refers to trauma-induced changes in brain functioning, typically caused by a blow to the head. The injury affects the functioning of neurons and causes disorientation or loss of consciousness. Symptoms of concussion can include headache, dizziness, nausea, impaired coordination, and sensitivity to light. Following a concussion, physicians recommend resting, minimizing stimulation or mental challenge, and refraining from any activity that can produce subsequent head injury (Harmon et al., 2013). Symptoms of a concussion are usually temporary, lasting no longer than a few weeks; however, in some cases they persist for much longer. Amnesia for events prior to a concussion appears to be a strong predictor of severity of impairment following a concussion (Dougan, Horswill, & Geffen, 2014).
Critical Thinking
· A 28-year-old soldier with six separate blast-related concussions reports that he has daily headaches and difficulty performing simple mental tasks.
· After a bomb explosion hurled an Army enlistee against a wall, he continued working despite being dazed and suffering shrapnel wounds. Confusion, headaches, and problems with balance persisted for months; he later developed seizures.
· The driver of a vehicle hit by a roadside bomb did not appear to be seriously injured. However, in the months following the explosion, his speech was slurred and he had difficulty reading and completing simple tasks. (T. C. Miller & Zwerdling, 2010)
A confidential survey conducted by the Rand Corporation (2010) revealed that almost 20 percent of veterans returning from Iraq and Afghanistan reported experiencing probable traumatic brain injury (TBI) during combat; injuries often involved blasts from hidden land mines and improvised explosive devices. These explosions cause complex brain damage, including (a) scattered brain injury resulting from shock waves that bruise the brain and damage nerve pathways, (b) penetrating injury from fragments of shrapnel or flying debris, and (c) injury from being thrown by the blast (Champion, Holcomb, & Young, 2009). Just what are the long-term risks from head injuries sustained in combat? The answer depends on many factors, including the source, location, and intensity of the injury, as well as interventions following the injury. Civilians treated for TBI are encouraged to allow the brain to rest to facilitate full recovery. However, in combat situations, mild head injuries are often not recognized, documented, and treated; soldiers frequently return immediately to combat (Murray et al., 2005).
Soldiers may not be receiving quality, evidence-based care for their brain injuries in a timely manner (T. C. Miller & Zwerdling, 2010). Additionally, because the long-term consequences of brain injury resulting from blast exposure are unknown, some researchers wonder if soldiers exposed to multiple blast injuries are at risk for degenerative neurocognitive conditions such as chronic traumatic encephalopathy (Rosenfeld et al., 2013). Researchers also stress the importance of intervening with the depressive and post-traumatic stress symptoms that frequently occur in military personnel who have experienced a TBI (Vasterling et al., 2012).
Should standard recommendations for TBI for civilians also apply to soldiers? What protocols might be beneficial to ensure that soldiers in combat receive appropriate care for TBI sustained in battle?
Did You Know?
Concussion is most prevalent among boys who participate in football, wrestling, rugby, hockey, and soccer. Girls have a 70 percent higher concussion rate than boys in “gender-comparable” sports, with the greatest risk of concussion occurring in soccer and basketball.
Source: American Academy of Neurology, 2013; Marar, McIlvain, Fields, & Comstock, 2012
It is estimated that U.S. children and adults incur almost 4 million concussions per year while involved in competitive sports or recreational activities; however, approximately half of these concussions go unreported. Having one concussion increases the likelihood of sustaining another concussion and requiring a longer period of recovery (Harmon et al., 2013).
A
cerebral contusion
(bruising of the brain) results when the brain strikes the skull with sufficient force to cause bruising. Unlike the disruption in cellular functioning seen in a concussion, contusions involve actual tissue damage in the areas bruised. Symptoms are similar to those seen with a concussion. Contusions and concussions commonly occur together. When someone receives a blow to the head, brain injury often occurs both at the site of impact and on the opposite side of the brain (i.e., the initial blow causes the brain to move and hit the other side of the skull). Neuroimaging can detect brain damage and monitor swelling. Unfortunately, brain imaging cannot always detect the more subtle changes caused by damage to neurons (a concussion), mild bruising of brain tissue (a contusion), or mild bleeding within the brain.
A
cerebral laceration
is an open head injury in which brain tissue is torn, pierced, or ruptured, usually from a skull fracture or an object that has penetrated the skull. As with a contusion, damage is localized and immediate medical care focuses on reducing bleeding and preventing swelling. As with other brain injuries, symptoms of cerebral lacerations can be quite serious, depending on the extent of damage to the brain tissue, the amount of hemorrhaging or swelling within the brain, and the medical care received. Severe brain trauma can have long-term effects, and, as you saw in the introductory case studies, recovery does not always ensure a return to prior levels of functioning. Along with the physical or cognitive difficulties produced by the injury, sleep difficulties and emotional symptoms commonly associated with TBI (e.g., depression, anxiety, irritability, or apathy) can also affect recuperation (Bryan, 2013).
Traumatic Brain Injury Among Combat Veterans
John Barnes incurred a traumatic brain injury in Iraq when mortar shrapnel entered his brain. Due to extensive damage involving his frontal lobe, he continues to exhibit impulsive behavior and lack of inhibition.
Whitney Shefte/The Washington Post/Getty Images
A type of brain injury receiving considerable media attention,
chronic traumatic encephalopathy
(CTE), is a progressive, degenerative condition diagnosed when autopsy reveals diffuse brain damage resulting from ongoing head trauma. CTE occurs in individuals who have had multiple episodes of head injury, such as athletes or those who serve in the military (Baugh et al., 2012). CTE is associated with psychological symptoms such as depression and poor impulse control, as well as a significantly increased risk of dementia. Symptoms associated with different stages of CTE include the following (McKee et al., 2013):
· Stage I—headache and loss of attention and concentration
· Stage II—depression, explosive outbursts, and short-term memory loss
· Stage III—cognitive impairment, including difficulties with planning and impulse control
· Stage IV—dementia, word-finding difficulty, and aggression
Did You Know?
Men who played in the NFL for at least 5 years are 3 times more likely to die from a neurodegenerative disorder such as Alzheimer’s or Parkinson’s disease than are other members of the U.S. population.
Source: Lehman, Hein, Baron, & Gersic, 2012
Similar to the neurodegenerative disorders we discuss later in the chapter, the neurological damage associated with CTE progresses slowly over decades, eventually resulting in dementia.
Case Study
Kate McCarron’s stroke symptoms started on a Friday, with a little tingle in her leg. On Saturday, McCarron, age 46, felt uncharacteristically tired. Sunday she seemed a bit under the weather. Monday, her left side felt numb. Tuesday morning, she couldn’t move her left side. She was rushed to the hospital. A small blood vessel leading to a deep part of her brain was closing, choking off a region of her brain that controlled motion (A. Dworkin, 2009).
Vascular neurocognitive disorders
can result from a one-time
cardiovascular
event such as a stroke or from unnoticed, ongoing disruptions to blood flow within the brain. Predominant cognitive symptoms of vascular neurocognitive disorder involve difficulties with complex attention, information processing, planning, and problem solving. Changes in motivation, personality, or mood are also common. Vascular neurocognitive disorders often begin with
atherosclerosis
, thickening of the arteries resulting from a buildup of plaque. This plaque (composed of fat, cholesterol, and other substances) accumulates over time, thickens, and narrows artery walls; the result is reduced blood flow to the brain and other organs.
Critical Thinking
How important is it for those involved in sports to know about concussion? Injuries resulting from team sports are increasingly sparking public concern. The suicides of Pennsylvania college football player Owen Thomas, age 21, and NFL linebacker Junior Seau, age 43, garnered attention when their autopsies revealed evidence of the degenerative brain condition chronic traumatic encephalopathy (CTE), likely resulting from chronic head injury incurred while playing football. An autopsy on former Cincinnati Bengals player Chris Henry, age 26, who died after falling out of a truck, also revealed CTE. Amazingly, none of these athletes were ever diagnosed with a concussion during their years in football. How could such significant brain damage occur at such a young age, particularly with no history of concussion?
A groundbreaking study involving a high school football team (Talavage et al., 2010) shed some light on the issue. Researchers compared cognitive testing and brain imaging of the players (obtained before, during, and after the football season) with data regarding the frequency and intensity of head impact during the football season (obtained by equipping the players’ helmets with special impact-monitoring sensors). As expected, players who had experienced a concussion during the season showed MRI changes and related cognitive declines. However, so did half of the other players; data from the impact-monitoring sensors revealed that the players who experienced brain changes but no recorded concussions had sustained multiple impacts during the season. For example, one affected player had experienced 1,600 significant head blows during the season.
A similarly designed study involving college varsity football and ice hockey players wearing instrumented helmets revealed that those with more measured physical contact and head impact showed deterioration in performance on tests involving verbal learning and reaction time. The researchers concluded that repetitive head impact throughout a single sports season has the potential to impair learning in college athletes (McAllister et al., 2012).
Professional medical organizations have created guidelines for school-age athletes suspected of having a concussion. Recommendations include immediate removal from play and restriction of physical activity for at least 7–10 days. Return to play should occur only after all acute symptoms subside and a health professional knowledgeable about head injury agrees that it is safe to resume athletic activities (American Academy of Neurology, 2013). If followed, these guidelines could significantly increase safety for athletes. Careful monitoring of athletes with possible neurological damage (e.g., headache, confusion, poor balance, speech, vision, or hearing difficulties) is certainly a step in the right direction. Unfortunately, it is also recognized that some athletes deny concussion symptoms so they can continue playing even when they know the risks (Strand, 2013). Are there adequate protections in place for those who experience a blow to the head but show no symptoms of a concussion? Are the potential dangers of head injuries in sports such as basketball, soccer, baseball, hockey, or cycling receiving sufficient attention?
A
stroke
occurs when there is an obstruction in blood flow to or within the brain; the sudden halt of blood flow results in death of neurons and loss of brain function. There are two major types of strokes: hemorrhagic strokes and ischemic strokes. A
hemorrhagic stroke
, unrelated to plaque buildup, occurs when a blood vessel bursts and bleeds into the brain. An
ischemic stroke
is caused by a clot or severe narrowing of the arteries; approximately 87 percent of strokes are ischemic (Go et al., 2013). A
transient ischemic attack (TIA)
is a “mini-stroke” or “warning stroke” resulting from temporary blockage of blood vessels in the brain; symptoms often last for only a few minutes. Seeking medical attention for transient stroke symptoms is important because these episodes often precede an ischemic stroke (Gupta, Farrell, & Mittal, 2014). When people seek emergency medical care for stroke symptoms, medications can dissolve the clot and prevent serious brain damage. In both ischemic and hemorrhagic strokes, brain damage occurs when brain cells die due to lack of blood, oxygen, and nutrients (
Figure 12.3
).
Figure 12.3Types of Stroke
Ischemic strokes resulting from a blocked artery account for approximately 87 percent of all strokes.
© Cengage Learning®
Strokes can occur at any age; in fact, approximately one third of those people who experience a stroke each year are under age 65 (Hall, Levant, & DeFrances, 2012). Immediate medical attention and careful management of neurological complications from stroke (e.g., bleeding or swelling within the brain) reduces mortality and improves prognosis (Balami, Chen, & Grunwald, 2011). However, stroke remains the fourth leading cause of death in the United States; stroke risk and mortality from stroke are particularly high for African Americans (Go et al., 2013).
Those younger than 50 years of age who experience a stroke often have risk factors such as hypertension, diabetes, high cholesterol, smoking, or exposure to secondhand smoke (Balci, Utku, Asil, & Celik, 2011). Cigarette smoking is a major contributor in about 1 in 4 strokes; however, when young adults experience a stroke, the contribution of smoking approaches 50 percent. An analysis of worldwide data revealed that men and women who smoke have a 60–80 percent increase in stroke risk; the risk of having a deadly hemorrhagic stroke is particularly high for women who smoke (Peters, Huxley, & Woodward, 2013).
Use of oral contraceptives (i.e., “the pill”) can increase stroke risk, particularly when combined with smoking (Raval, Borges-Garcia, Diaz, Sick, & Bramlett, 2013). Worldwide data regarding stroke risk point to stress, poor eating and sedentary lifestyles, and heavy or binge drinking as other major contributors to stroke (O’Donnell et al., 2010). Additionally, depression is associated with a 34 percent increase in risk for stroke; it is possible that unhealthy lifestyle factors associated with both disorders are the cause of this increased risk (Pan, Sun, Okereke, Rexrode, & Hu, 2011).
Stroke is not only a leading cause of death but also a significant cause of disability (J. A. Young & Tolentino, 2011). Prompt medical intervention decreases the chances of death and vastly improves prognosis (Saver et al., 2013); this underscores the importance of recognizing signs of a stroke (
Table 12.6
). Because many people do not recognize stroke symptoms (e.g., slurred speech, blurry vision, or numbness on one side of the body), or hesitate to treat these symptoms as an emergency, public health campaigns continue to stress the importance of immediate intervention. Additionally, many are unaware that women may display unique stroke symptoms, including sudden nausea, hiccups, facial pain, overall weakness, and shortness of breath (National Stroke Association, 2014).
Table 12.6
|
Emergency medical attention immediately following the onset of stroke symptoms can significantly improve outcomes for both ischemic and hemorrhagic strokes. |
|
· Numbness or weakness, including drooping of facial features or weakness on one side of the body |
|
· Confusion or difficulty understanding questions or conversation |
|
· Slurred or incoherent speech |
|
· Vision difficulty in one or both eyes |
|
· Sudden dizziness, loss of balance, or difficulty with coordination |
|
· Severe headache with no known cause |
© Cengage Learning®
Did You Know?
Depressed women had a 2.4 times increased risk of stroke compared to those who were not depressed, according to a longitudinal study of over 10,000 middle-aged women.
Source: Jackson & Mishra, 2013
Stroke survivors who do not receive immediate intervention often require long-term care because residual physical and psychological symptoms impair independent functioning. Strokes damaging the left side of the brain typically affect speech and language proficiency, as well as physical movement on the right half of the body. Strokes occurring within the right hemisphere can increase impulsivity and impair judgment, short-term memory, and motor movement on the left side of the body. Visual problems (blurry or double vision) may occur in those with a right-hemisphere stroke. Cognitive, behavioral, and emotional changes that occur following stroke depend not only on the extent of brain damage but also on the individual’s personality, emotional resilience, and coping skills. Some stroke survivors experience frustration and depression, whereas others actively and optimistically participate in therapeutic rehabilitation activities.
A series of small asymptomatic (symptomless) strokes due to small bleeds in the brain or a decrease in blood flow from small clots or narrowed arteries can cause small pockets of dead brain cells. The resulting brain damage may lead to deterioration in intellectual and physical abilities. Surprisingly, these mini-strokes may affect up to 25 percent of older adults (Blum et al., 2012). The severity of symptoms depends on the extensiveness of damage and the brain regions involved (Poels et al., 2012). Brain damage from small strokes, estimated to cause 8–15 percent of all dementia, often coexists with Alzheimer’s disease because both have similar risk factors such as hypertension, diabetes, and smoking (Nobel, Mayo, Hanley, Nadeau, & Daskalopoulou, 2014).
Results of a Stroke on the Brain
The brain damage associated with a stroke is caused by blockages that cause an interruption in the brain’s blood supply or by the leakage of blood through blood vessel walls. Here, a three-dimensional magnetic resonance angiogram scan shows a human brain after a hemorrhagic stroke. Major arteries are shown in white. The central region in yellow is an area in which bleeding occurred.
Zephyr/Science Source
Use or abuse of drugs or alcohol can result in delirium or more chronic brain dysfunction. Delirium is associated with extreme intoxication, drug or alcohol withdrawal, use of multiple substances, or inhalant use (due to oxygen deprivation or the toxicity of substances inhaled). Symptoms consistent with mild neurocognitive disorder are common in individuals with a history of heavy substance use (APA, 2013). The symptoms usually continue during initial abstinence, but may improve with time. For example, many of the deficits associated with alcohol-induced neurocognitive disorder require a full year of abstinence before they fully subside (Stavro, Pelletier, & Potvin, 2013).
Case Study
Elizabeth R., a 46-year-old woman diagnosed with Alzheimer’s disease, is trying to cope with her increasing memory difficulties. She writes notes to herself and rehearses conversations, anticipating what might be said. After reading only a few sentences, she forgets what she has read. She sometimes forgets where the bathroom is located in her own house and is depressed by the realization that she is becoming a burden to her family (M. Clark et al., 1984, p. 60).
Alzheimer’s disease (AD)
, the most prevalent neurodegenerative disorder, involves a pattern of progressive cognitive decline. Although the main feature of AD is memory impairment, clinicians avoid diagnosing AD based solely on memory difficulties. Individuals seeking treatment for impaired memory develop AD at a rate of 12–15 percent per year; however, individuals with memory impairment in the general population (i.e., not just those who seek treatment) are less likely to develop AD, and in some cases show a reversal of symptoms (APA, 2013). Clear physiological indicators (e.g., evidence of genetic mutations or brain changes associated with AD) are required to predict which patients with mild memory impairment will likely develop AD (Ballard, Corbett, & Jones, 2011). Using the newest guidelines, a clinician can diagnose mild or major neurocognitive disorder due to AD by incorporating biological data such as genetic testing into the diagnostic process or by looking only at evidence of declines in cognitive and self-help skills (Howe, 2013).
Focus on Resilience
Given the serious consequences of neurocognitive disorders, you may wonder: “Is there anything that can be done to reduce the chances of experiencing a stroke, suffering a head injury, or developing a degenerative disorder?” The answer is yes, especially when prevention efforts begin at an early age. For example, the use of car seats and seat belts can help prevent head injury, as can the use of safe practices and properly fitting protective headgear during sports (Rivara et al., 2011). Similarly, allowing the brain to rest and recover after a blow to the head or a concussion can reduce the likelihood of long-term brain damage (American Academy of Neurology, 2013).
Kevin Peterson/Photodisc/Getty Images
Lifestyle changes focused on maintaining a healthy cardiovascular system such as exercising regularly and eating a well-balanced diet also reduce the risk of both stroke and dementia (Lövdén, Xu, & Wangy, 2013). Varied exercise of higher intensity or longer duration enhances neuroprotective effects and helps prevent cognitive decline in older adults (Kirk-Sanchez & McGough, 2014). A healthy lifestyle protects against dementia not only by reducing risk factors but also by promoting neurogenesis, the formation of new brain cells (Lazarov, Mattson, Peterson, Pimplika, & van Praag, 2010). Prevention efforts focus on modifiable risk factors (e.g., avoiding smoking and excessive consumption of salt, sugar, saturated fats, and alcohol), because these unhealthy behaviors account for almost 90 percent of the risk of stroke (Hankey, 2011) and much of the risk of dementia (L. D. Baker et al., 2010). Preventing or treating hypertension is a key modifiable risk factor associated with cognitive decline and dementia (Gasecki, Kwarciany, Nyka, & Narkiewicz, 2013). Regular participation in cognitively stimulating activities across the life span (especially during early and middle adulthood) is also associated with fewer pathological brain changes (less beta-amyloid) later in life (Landau et al., 2012). Prevention efforts really can make a difference in maintaining brain health.
AD affects more than 5 million Americans. It is estimated that by 2030 over 7 million adults in the United States will have AD, with the prevalence reaching 13.8 million by 2050 (Hebert, Weuve, Scherr, & Evans, 2013). Although AD can strike adults in midlife, risk of the disease significantly increases with age; those who are 65 have a 1 percent risk, whereas those who are 95 have a 40–50 percent risk (X. P. Wang & Ding, 2008). The prevalence and the severity of AD symptoms are greater among women than men, but the reasons for this difference are not fully understood (Mielke, Vemuri, & Rocca, 2014).
Characteristics of Alzheimer’s Disease
Memory and learning impairments associated with AD develop quite gradually, followed by a progressive decline in other areas of cognitive functioning. Unfortunately, the physiological processes that produce AD begin years before the onset of symptoms (Howe, 2013). As early symptoms—memory dysfunction, irritability, and cognitive impairment—gradually worsen, other symptoms such as social withdrawal, depression, apathy, delusions, impulsive behaviors, and neglect of personal hygiene often appear. Some individuals with AD become loving and childlike, whereas others become increasingly agitated and combative. At present, no curative or disease-reversing interventions exist for AD.
As we saw in the case of Elizabeth, deterioration of memory is one of the most disturbing symptoms for those who have AD and for their family members. Initially, those affected may forget appointments, phone numbers, and addresses, but as AD progresses, they lose track of the time of day, have trouble remembering recent and past events, and forget who they are. Even when memory is gone, however, emotions remain. In fact, researchers have found that although those with AD may forget details of an emotional event (such as the plot of a sad movie), the emotions of the experience continue (Feinstein, Duff, & Tranela, 2010).
Other Factors Affecting Memory Loss
A common concern of older adults is whether occasional memory lapses are signs of AD. Memory loss occurs for a variety of reasons. In some cases, it is an early symptom of AD. However, occasional lapses of memory are common in healthy adults. As we age, neurons are gradually lost, our brains become smaller, and we process information more slowly. Thus, occasional difficulty with memory or learning new material is normal. Many older adults experience only minimal decline in cognitive function; this is because, as we age, we continue to generate new brain cells and the brain reorganizes itself in a way that maximizes cognitive efficiency (Moran, Symmonds, Dolan, & Friston, 2014).
Did You Know?
Among families with a genetic mutation responsible for early-onset Alzheimer’s disease, changes in the brain and nervous system have been detected in individuals as young as 18 years of age.
Source: Reiman et al., 2012
Memory loss and confusion can also result from temporary conditions such as infections or reactions to prescription drugs. Medications sometimes interact with one another or with certain foods to produce side effects, including memory impairment. In addition, various physical conditions and nutritional deficiencies can produce memory loss and symptoms resembling dementia. This type of memory loss usually disappears once the medical condition is diagnosed and treated.
Did Alzheimer’s Disease Affect His Presidency?
Former president Ronald Reagan was treated for a traumatic head injury after being thrown from a horse. Five years later, he was diagnosed with Alzheimer’s disease at age 83. Symptoms of the disease, such as memory difficulties, began while he was still in office. Some speculate that his head injury accelerated the progression of his Alzheimer’s disease.
AP Images/Ron Schumacher
Alzheimer’s Disease and the Brain
Individuals with AD exhibit a variety of changes in the brain. First, those with end-stage AD have marked shrinkage of brain tissue due to the widespread death of neurons. Second, autopsies of people with AD reveal two abnormal structures— neurofibrillary tangles and beta-amyloid plaques. Both affect metabolic processes and health of neurons in the hippocampus and in areas of the cortex associated with memory and cognition.
Neurofibrillary tangles
, found inside nerve cells, are composed of twisted fibers of tau, a protein that helps transport nutrients in healthy cells; in those with AD, biochemical alterations in tau proteins result in cellular dysfunction.
Beta-amyloid plaques
develop when beta-amyloid proteins aggregate in the spaces between neurons (see
Figure 12.4
). Neurofibrillary tangles and beta-amyloid plaques are associated with decreased neurogenesis, as well as inflammation, loss of cellular connections, and other changes that eventually result in the death of neurons and shrinking of the brain (Lazarov, Mattson, Peterson, Pimplika, & van Praag, 2010).
Figure 12.4Brain Changes Associated with Alzheimer’s Disease
Autopsies of the brains of individuals with Alzheimer’s disease reveal beta-amyloid plaques in the spaces between neurons and neurofibrillary tangles inside nerve cells. These brain changes begin years before symptoms of the disease appear.
© Cengage Learning®
Brain changes associated with AD appear years before dementia develops (Bernard et al., 2014). First, beta-amyloid deposits appear; as these plaques multiply, neurodegeneration begins. Next, mild cognitive symptoms develop, usually followed by progressive cognitive decline and impairment in daily functioning (Blaze, 2013). We are learning more about this process due to recent advances in positron emission tomography (PET) imaging involving tracers that attach to beta-amyloid proteins, thus allowing the detection and monitoring of beta-amyloid plaques in the living brain (Johnson et al., 2013). Additionally, new fluorescent compounds are allowing PET imaging of tau protein clusters and neurofibrillary tangles in the brains of people with AD and other neurodegenerative disorders (Mathis & Klunk, 2013). It appears that tau creates brain changes more rapidly than beta-amyloid plaques and that beta-amyloid plaques somehow accelerate the spread of tau within the brain (Jack & Holtzman, 2013).
Did You Know?
Individuals with Alzheimer’s disease had 4 times more residue from the pesticide DDT (banned in 1971) in their blood compared to healthy adults of a similar age.
Source: Richardson et al., 2014
It is still not possible to definitively diagnose AD before autopsy, even when a person has multiple indicators suggestive of AD (e.g., memory loss, brain scans showing brain shrinkage). Although the monitoring of tau and beta-amyloid proteins in cerebrospinal fluid (CSF), the liquid that surrounds the brain and spinal cord, and the detection of beta-amyloid plaques via PET imaging are used for research, these biological markers are not sufficiently sensitive or accurate to make an AD diagnosis (Blaze, 2013).
A number of factors increase the risk of AD, including both hereditary and environmental influences. We are learning more about genetic influences on AD. Our bodies produce a chemical, apolipoprotein E (ApoE), that helps clear beta-amyloid by-products from the brain. The gene associated with this process (the APOE gene) has three variants (alleles). One of these variants, the e4 allele of the APOE gene, appears to decrease production of ApoE thus increasing risk for AD. Although the APOE-e4 allele increases the likelihood of developing AD and contributes to approximately 25 percent of all AD, people with this genotype do not necessarily develop AD; however, risk is further increased when the APOE-e4 allele is inherited from both parents.
Continuum
Video Project
Myriam© Cengage Learning®
Alzheimer’s Disease
“I’m going to forget their names. I’m going to forget who they are. Alzheimer’s is eating away at my brain.”
Access the Continuum Video Project in MindTap at www.cengagebrain.com
Researchers have also identified three rare genetic mutations (deterministic genes) that result in autosomal-dominant Alzheimer’s disease; these genes are responsible for the multigenerational inheritance of early-onset AD in some families (Pilotto, Padovani, & Borroni, 2013). Those affected by these mutations usually develop AD in midlife, sometimes as early as the mid-30s. People who inherit these mutations appear to produce large quantities of a stickier version of the beta-amyloid protein that exits more slowly from the brain (Potter et al., 2013). Genetic association studies involving AD are shedding light on other genetic pathways and possible biological mechanisms underlying the disorder (Medway & Morgan, 2014). Interestingly, some carriers of genes associated with AD have shown neurological abnormalities in brain pathways associated with AD but no overt symptoms (Lampert, Choudhury, Hostage, Petrella, & Doraiswamy, 2013). As you might imagine, following the progression of biomarkers in asymptomatic individuals is of great interest to researchers.
Lifestyle variables associated with stroke and cardiovascular disease also increase risk of AD. Researchers interested in determining how dietary intake affects beta-amyloid studied older adult volunteers who were randomly assigned to consume a diet either high or low in saturated fat; the high-fat diet resulted in increases in circulating beta-amyloid and reductions of ApoE, the chemical that helps clear the brain of beta-amyloid by-products (Hanson et al., 2013). Conversely, low levels of “bad” (LDL) cholesterol and high levels of “good” (HDL) cholesterol are associated with fewer beta-amyloid deposits in the brain (Reed et al., 2013). Another environmental factor we have already mentioned as associated with AD is traumatic brain injury (APA, 2013).
Alzheimer’s Disease
As can be seen in these PET scans comparing brain activity between someone with Alzheimer’s disease and a healthy control, Alzheimer’s disease causes degeneration and death of nerve cells and significantly reduces metabolic activity in the brain. The associated brain dysfunction results in symptoms such as memory loss, disorientation, and personality change.
Dr. Robert Friedland/Science Source
There is also a link between sleep and the amount of beta-amyloid in the brain. Older adult volunteers who report poor sleep quality or quantity had more beta-amyloid deposits in the brain compared to those reporting adequate sleep (Spira et al., 2013). Additionally, in a group of asymptomatic individuals involved in an ongoing study, those with evidence of beta-amyloid abnormalities had the poorest documented sleep quality (Ju et al., 2013). These findings are consistent with data suggesting that beta-amyloid and other proteins are cleared from the brain during sleep. Researchers are attempting to determine if the buildup of beta-amyloid plaque disrupts sleep, or if loss of sleep contributes to the development of beta-amyloid plaques. Efforts to better understand the genes and biological processes associated with AD continue, with the hope that someday we will be able to prevent or treat this devastating disease (Bateman et al., 2011).
12-2eNeurocognitive Disorder due to Dementia with Lewy Bodies
Dementia with Lewy bodies (DLB)
, the second most common form of dementia, results in cognitive decline combined with the development of unusual movements similar to those seen in Parkinson’s disease, a disorder we discuss later in the chapter. Characteristics of DLB include (a) significant fluctuations in attention and alertness (e.g., staring spells and periods of extreme drowsiness); (b) recurrent, detailed visual hallucinations; (c) impaired mobility (frequent falls, a shuffling gait, muscular rigidity, and slowed movement) that occurs after the onset of cognitive decline; and (d) sleep disturbance, including acting out dreams. Depression is common among those with DLB. Compared to the cognitive deficits associated with AD, memory and language skills are usually more intact in those with DLB, whereas visual-spatial tasks (such as reproducing a drawing) are more impaired. Although DLB tends to develop more rapidly than AD, the two diseases have a similar survival period of approximately 8 years after diagnosis (Lewy Body Dementia Association, 2014).
Did You Know?
Depression is associated with an increased risk of Alzheimer’s disease and other dementias perhaps because depression and dementia have similar risk factors (e.g., poor diet, little exercise). Some researchers contend that depression that begins later in life may represent an early symptom of cognitive decline.
Source: G. Li et al., 2011; Spira, Rebok, Stone, Kramer, & Yaffe, 2012
Individuals with DLB have brain cell irregularities, called Lewy bodies, which result from the buildup of abnormal proteins in the nuclei of neurons. These unique cell structures (named after Frederick Lewy, who first discovered them) are also present in Parkinson’s disease. When Lewy bodies develop in the cortex, they deplete the neurotransmitter acetylcholine, resulting in the perceptual, cognitive, and behavioral symptoms seen in DLB and in later stages of Parkinson’s disease. Lewy bodies in the brain stem cause the depletion of dopamine and the motor dysfunction seen in Parkinson’s disease and later stages of DLB.
The incidence of DLB increases with age and occurs more frequently in men (Savica et al., 2013). DLB may account for up to 30 percent of all dementias; however, prevalence data may be inaccurate because of the overlap in symptoms with other neurodegenerative disorders and because DLB can only be confirmed by autopsy (National Institute of Neurological Disorders and Stroke, 2014). Additionally, professionals who are not dementia specialists are often less familiar with DLB. Although researchers have not yet identified any genes associated with DLB, the disorder occurs more frequently in some families (Nervi et al., 2011).
Frontotemporal lobar degeneration (FTLD)
, the fourth leading cause of dementia, is characterized by progressive declines in language or behavior; these deficits result from degeneration and atrophy in the frontal and temporal lobes of the brain (Galimberti & Scarpini, 2012). FTLD has several variants that involve either behavioral or language abnormalities. Symptoms associated with these variants include (a) significant changes in behavior, personality, and social skills (e.g., impulsive or uninhibited actions, apathy, loss of empathy, stereotyped behavior patterns, or overeating); or (b) progressive difficulty with fluent speech or word meaning (e.g., understanding words or naming objects). Muscle weakness or other motoric abnormalities are sometimes present. There is usually minimal decline in learning, memory, or perceptual-motor skills. Behavioral symptoms are associated with atrophy in the frontal lobe, whereas communication symptoms occur when temporal lobe damage is predominant (APA, 2013).
The average age of onset is between 45 and 64 years of age, making FTLD the second leading cause of early-onset dementia. Neuroimaging can assist with diagnosis by documenting the atrophy in the frontal or temporal lobes characteristic of FTLD (Association for Frontotemporal Degeneration, 2014). Genetic mutations appear to contribute to FTLD, with up to 40 percent of individuals with FTLD reporting a family history of neurodegenerative illness (Seltman & Matthews, 2012).
12-2gNeurocognitive Disorder due to Parkinson’s Disease
Parkinson’s disease (PD)
involves four primary symptoms: (a) tremor of the hands, arms, legs, jaw, or face; (b) rigidity of the limbs and trunk; (c) slowness in initiating movement; and (d) drooping posture or impaired balance and coordination (National Institute of Neurological Disorders and Stroke, 2014). As the disease progresses, motor tremors and incoordination can interfere with daily activities. In neurocognitive disorder due to PD, motor symptoms are evident at least 1 year prior to notable cognitive decline. Mild cognitive impairment often develops early in the course of PD and affects about 27 percent of those with the disorder (Litvan et al., 2012); the dementia commonly seen in the later stages of PD results in cognitive and behavioral symptoms similar to those seen in DLB (Lewy Body Dementia Association, 2014). Personality and mood changes including apathy, depression, or anxiety, as well as hallucinations and delusions, occur with PD (APA, 2013). The severity and progression of symptoms varies significantly from person to person.
PD is the second most common neurodegenerative disorder in the United States, affecting about 630,000 individuals with the prevalence expected to double by 2040 (Kowal, Dall, Chakrabarti, Storm, & Jain, 2013). The prevalence of PD increases with age and affects 3 percent of those older than 85. PD strikes more men than women, but the reasons for this discrepancy are unclear (APA, 2013). The symptoms of PD result from the accelerated aging of neurons and the death of dopamine-producing neurons in the midbrain, as well as the presence of Lewy body proteins in the motor area of the brain stem (Sharma et al., 2013).
Parkinson’s Disease
Actor Michael J. Fox, who was diagnosed with Parkinson’s disease in 1991, performs at a benefit for the Michael J. Fox Foundation for Parkinson’s Research.
Mike Coppola/Getty Images Entertainment/Getty Images
Because genetic mutations account for only 5 percent of PD cases, researchers are trying to learn more about what causes the pattern of brain cell death seen in the disease (Trinh & Farrer, 2013). Twin studies have revealed that occupational exposure to certain toxins (contained in solvents and household cleaners) increases the risk of PD (Goldman et al., 2012). Exposure to herbicides and pesticides also appears to increase the likelihood of developing PD (APA, 2013). The disorder occurs more frequently in the northern Midwest and the Northeast and in urban settings; this geographic distribution has raised questions about whether environmental toxins common to these areas are associated with the development of PD (A. W. Willis, Bradley, et al., 2010).
Huntington’s disease (HD)
is a rare, genetically transmitted degenerative disorder characterized by involuntary movement, progressive dementia, and emotional instability. Age of onset is variable, ranging from childhood to late in life; onset most typically occurs during midlife (APA, 2013). Initial symptoms often involve neurocognitive decline and changes in personality and emotional stability. The progressive cognitive deficits associated with HD typically begin with difficulties involving complex attention, planning, and problem solving. Additionally, many individuals with HD become uncharacteristically apathetic, moody, and quarrelsome. As the disorder progresses, physical symptoms such as facial grimaces, difficulty speaking, and abrupt, repetitive movements often develop. Eventually, the severity of motor and cognitive impairment results in total dependency and the need for full-time care. There is no effective treatment for HD; death typically occurs 15–20 years after the onset of symptoms (Clabough, 2013).
Did You Know?
Evidence of a genetic mutation that causes Huntington’s disease has been found in some individuals whose primary symptom is major depression.
Source: Perlis, Smoller, et al., 2010
Because HD is transmitted from parent to child through a dominant genetic mutation, offspring of someone with HD have about a 50/50 chance of developing the disorder. Predictive genetic testing is available for family members who want to know if they will develop HD. Additionally, neuroimaging to monitor glucose metabolism in the cortex can help predict rate of disease progression in those with HD (Shin et al., 2013). Genetic counseling is extremely important in preventing transmission of the disease.
2-2iNeurocognitive Disorder due to HIV Infection
Many people know about the serious complications associated with HIV infection and AIDS (acquired immune deficiency syndrome), including susceptibility to diseases, physical deterioration, and death. Relatively few people realize that cognitive impairment is sometimes the first sign of untreated HIV infection. Symptoms can vary significantly but often include slower mental processing, difficulty with complex mental tasks, and difficulty concentrating or learning new information (APA, 2013). In serious cases, a diagnosis of AIDS dementia complex (ADC) is made. ADC, a major neurocognitive disorder, develops when HIV becomes active within the brain resulting in significant alteration of mental processes. HIV-related infection can also produce inflammation throughout the brain and central nervous system.
Although the antiretroviral therapies used to treat HIV infection and AIDS can prevent or delay the onset of the severe cognitive dysfunction associated with ADC, HIV-related brain changes still occur in almost half of those taking antiretroviral medications. For example, neuroimaging studies revealed that 33 percent of one group receiving treatment had HIV-related neurological changes but without symptoms of cognitive decline; in addition, 12 percent of the group had mild neurocognitive impairment and 2 percent had ADC. The percentages of those affected were even higher when individuals with comorbid conditions were included (Heaton et al., 2010). Researchers hope that the prevalence of HIV-related neurocognitive disorder will decrease once antiretroviral medications are able to efficiently penetrate the brain and central nervous system (Vassallo et al., 2014).
Controversy
Genetic Testing: Helpful or Harmful?
DNA testing is now available to provide information regarding risk for a variety of neurocognitive disorders. Genotyping (gathering information about specific genes by examining an individual’s DNA) brings up a number of interconnected issues. When genotyping is performed on individuals who have a family member with a genetically determined condition such as Huntington’s disease (HD) or early-onset Alzheimer’s disease (AD), the outcome of the test reveals life-changing information—they know with certainty if they will develop the disorder afflicting their parent or other family members. In cases where genetic tests only indicate possible risk (e.g., the APOE-e4 genotype associated with later-onset AD), clinicians often discourage genetic testing due to concerns that knowledge of possible risk can be more harmful than helpful (Howe, 2010). For example, someone who learns that he or she has the APOE-e4 genotype knows there is approximately a 25 percent chance of developing AD—not the 100 percent risk revealed through genotype analysis involving HD or early-onset AD.
Those who encourage genetic testing for individuals who may carry deterministic genes (e.g., when family members have HD or early-onset AD) emphasize benefits such as being able to plan for the future, including decisions about whether or not to have children. However, others discourage such testing because of the social and economic stigma associated with these conditions and the lack of specific treatments or interventions if gene mutations are detected (The Lancet Neurology, 2010). Those who support genetic testing when there is possible risk of AD (e.g., families who have the APOE-e4 genotype) believe that learning about an increased risk of AD may motivate lifestyle changes that ultimately reduce the risk of developing the disease. Additionally, individuals with the APOE-e4 genotype may be able to participate in research studies aimed at preventing or slowing the progression of AD (Sleegers et al., 2010). Once such interventions exist, some of the debate may subside.
For Further Consideration
1. If your parent had Huntington’s disease or early-onset Alzheimer’s disease, would you want to know if you would eventually develop the disorder?
2. If your family members had later-onset Alzheimer’s disease, would you want to know if you carried the APOE-e4 genotype and had a 25 percent risk of developing the disorder?
Checkpoint Review
1. What kinds of events can cause a traumatic brain injury?
2. What causes chronic traumatic encephalopathy?
3. What are some factors that increase the risk of having a stroke or developing a degenerative neurocognitive disorder?
12-3Treatment Considerations with Neurocognitive Disorders
Because neurocognitive disorders have many different causes and are associated with different symptoms and dysfunctions, treatment approaches vary widely. First, any underlying medical conditions are addressed. Beyond that, the major interventions for neurocognitive disorders include rehabilitation services, biological interventions, cognitive and behavioral treatment, lifestyle changes, and environmental support.
12-3aRehabilitation Services
The key to recovery for those affected by stroke or traumatic brain injury is participation in comprehensive, sustained rehabilitation services. Physical, occupational, speech, and language therapy help individuals relearn skills or compensate for lost abilities. A person’s commitment to and participation in therapy plays an important role in recovery. Depression, pessimism, and anxiety can stall progress. Fortunately, those participating in rehabilitation become encouraged when the brain begins to reorganize and skills return. Neuroimaging techniques are increasingly used to document brain changes achieved through rehabilitation; in fact, neuroimaging can help determine which physical and occupational therapies best enhance brain recovery (K. C. Lin et al., 2010).
12-3bBiological Treatment
Medications can help prevent, control, or reduce the symptoms of some neurocognitive disorders. Treating vitamin deficiencies can also improve or reduce symptoms in some conditions. For example, the persistent memory and learning difficulties seen in Wernicke-Korsakoff’s syndrome, a disorder caused by thiamine (vitamin B1) deficiencies associated with chronic alcohol abuse, can improve when nutritional supplements are provided during alcohol treatment (Isenberg-Grzeda, Kutner, & Nicolson, 2012). Higher blood levels of an amino acid, homocysteine, are also associated with increased risk of AD. Fortunately, certain vitamins, such as vitamin B6 or B12, can decrease cognitive impairment in some individuals with high homocysteine levels. MRI scans of individuals with mild cognitive impairment taking high doses of B vitamins over a 2-year period revealed that brain atrophy was slowed by about 30 percent; not surprisingly, atrophy was reduced most (up to 53 percent) in those with the highest initial levels of homocysteine (Smith et al., 2010).
Did You Know?
Speaking two languages appears to delay the age of onset of dementia by approximately 4 years. This may be because bilingualism increases the ability of the brain to continue functioning normally despite neurodegeneration.
Source: Alladi et al., 2013
Medications, including levodopa, a drug that increases dopamine availability, can provide relief from both cognitive and physical symptoms of PD; however, it can also produce problems with impulse control, hallucinations and other psychotic symptoms, and difficulty with voluntary motor movement (Poletti & Bonuccelli, 2013). Thus, physicians often delay pharmacological treatment for PD until it is certain that the benefits clearly outweigh the risks. For some patients, implanting electrodes that stimulate the brain produces symptom improvement (van Hartevelt et al., 2014). Gene therapy (administering genes into the brains of PD patients) is also being tested with PD patients with the goal of sufficiently modifying brain cells so that they once again produce dopamine (Palfi et al., 2014).
Effective Rehabilitation
Spc. Bob Westbrook is undergoing treatment at the Warrior Recovery Center for a traumatic brain injury he sustained while deployed in Afghanistan. The program uses multiple therapies, including computer applications that focus on improving attention and processing speed.
AP Images/Bryan Oller
The two classes of drugs (acetylcholinesterase inhibitors and memantine) approved to help slow the progression of AD have not shown robust effects (Howe, 2013). Efforts continue to focus on developing medications that might help prevent the development of beta-amyloid and tau protein irregularities in those at high risk for AD (Ghezzi, Scarpini, & Galimberti, 2013). Other proposed treatments for AD are still in the early stages, including deep brain stimulation to improve neural circuit function (Lyketsos, Targum, Pendergrass, & Lozano, 2012).
Antidepressants can also help alleviate the depression associated with stroke and other neurocognitive disorders. In one study, individuals with moderate to severe motor impairment resulting from an ischemic stroke took an antidepressant (fluoxetine) for 3 months. This group not only reported fewer depressive symptoms than did individuals in a placebo control group but also regained more muscle function; the antidepressant may have enhanced progress by reducing brain inflammation, improving neurotransmitter functioning, or enhancing participation in physical therapy due to improved mood (Chollet et al., 2011).
Although low doses of antipsychotic medication sometimes reduce symptoms associated with neurodegenerative disorders such as paranoia, hallucinations, and agitation, these medications are used cautiously, especially in older individuals (Declercq et al., 2013). As mentioned previously, it is often necessary to balance the positive effects and side effects of medications, taking particular care to monitor potential interactions of multiple medications.
12-3cCognitive and Behavioral Treatment
Cognitive deficits and emotional changes caused by neurocognitive disorders (e.g., emotional reactivity and diminished ability to concentrate) can hinder recovery and interfere with well-being. For example, depression, common among those with vascular neurocognitive disorder, can decrease follow-through with treatment recommendations and increase risk of subsequent strokes (Sibolt et al., 2013).
Psychotherapy can enhance coping and participation in rehabilitation efforts. For example, a cognitive-behavioral treatment targeting depression in individuals with PD included identifying life stressors and teaching the participants self-care, stress management, and relaxation techniques. The treatment was found to be both feasible and effective (Dobkin et al., 2006). Cognitive and behavioral therapy techniques can also reduce the frequency or severity of problem behaviors associated with neurocognitive disorders such as aggression or socially inappropriate conduct. Strategies may include teaching the individual social skills, reducing complex tasks (e.g., dressing or eating) into simpler steps, or simplifying the environment to avoid confusion and frustration. Additionally, preliminary research has demonstrated positive neurological changes including reduced brain atrophy in individuals with mild neurocognitive impairment who participated in meditation and mindfulness-based stress reduction (Wells et al., 2013).
12-3dLifestyle Changes
Lifestyle changes can help prevent or reduce progression of some neurocognitive disorders. Among one group of adults with early-stage AD, those with good cardiovascular fitness had less brain atrophy than those who did not exercise regularly (Honea et al., 2009). Treatment for vascular neurocognitive disorders often targets smoking cessation, weight reduction, and blood sugar, cholesterol, or blood pressure control (Peters, Huxley, & Woodward, 2013). Such changes may help also slow the progression of AD (Rolland, van Kan, & Vellas, 2010).
Increased social interaction and mental stimulation involving enjoyable, social activities that provide an opportunity to concentrate and use memory skills can improve communication skills and reduce cognitive decline in individuals with dementia (Woods, Aguirre, Spector, & Orrell, 2012). However, the use of specific cognitive training programs does not have strong research support, nor do the results of the training appear to generalize to daily living activities among those exhibiting cognitive decline (Lövdén, Xu, & Wangy, 2013).
12-3dLifestyle Changes
Lifestyle changes can help prevent or reduce progression of some neurocognitive disorders. Among one group of adults with early-stage AD, those with good cardiovascular fitness had less brain atrophy than those who did not exercise regularly (Honea et al., 2009). Treatment for vascular neurocognitive disorders often targets smoking cessation, weight reduction, and blood sugar, cholesterol, or blood pressure control (Peters, Huxley, & Woodward, 2013). Such changes may help also slow the progression of AD (Rolland, van Kan, & Vellas, 2010).
Increased social interaction and mental stimulation involving enjoyable, social activities that provide an opportunity to concentrate and use memory skills can improve communication skills and reduce cognitive decline in individuals with dementia (Woods, Aguirre, Spector, & Orrell, 2012). However, the use of specific cognitive training programs does not have strong research support, nor do the results of the training appear to generalize to daily living activities among those exhibiting cognitive decline (Lövdén, Xu, & Wangy, 2013).
