Ch.14, Neurocognitive Disorders Flashcards
brain cell deterioiration and regrowth
With a few exceptions, cell bodies and neural pathways in the brain do not appear to have the power of regeneration, which means that their destruction is permanent. When brain injury occurs in an older child or adult, there is a loss in established functioning. Often, the person who has sustained this loss is painfully aware of what he or she is no longer able to do, adding a pronounced psychological burden to the physical burden of having the lesion.
anosognosia
n other cases, the impairment may extend to the loss of capacity for realistic self-appraisal (a condition called anosognosia), leaving these patients relatively unaware of their losses and hence poorly motivated for rehabilitation.
Is the Inclusion of Mild Neurocognitive Disorder a Good Idea in the DSM 5?
An important addition to DSM-5 is the new diagnosis of mild neurocognitive disorder. This change reflects an effort to recognize that cognitive problems that do not reach the level of affecting everyday functioning may still warrant clinical attention. But this new diagnostic category is not without controversy.
Some people are concerned that the use of the word mild trivializes the cognitive impairments that are being experienced. It may also imply that there is no need for services to be provided. On the other hand, refraining from using a term like dementia until the cognitive impairment is more severe may alleviate anxiety and reduce stigma.
But if minor cognitive disorder is considered to be a prodromal stage before the onset of more severe impairment, will receiving the more mild diagnosis still not be a source of anxiety? People experiencing minor cognitive impairment (MCI is a descriptive term and not a DSM-5 diagnosis) are thought to be at increased risk for the development of Alzheimer’s disease. If these people can now be formally diagnosed with a disorder (unlike MCI, mild neurocognitive disorder is now an official diagnosis) will we be alarming large numbers of people needlessly?
-how do we separate mild neurocognitive disorder from normal aging?
diffuse vs focal brain damage
diffuse—or widespread—damage, such as might occur with moderate oxygen deprivation or the ingestion of toxic substances like mercury. Such a person may complain of memory problems due to an inability to sustain focused retrieval efforts, while his or her ability to store new information remains intact.
- focal brain lesions involve circumscribed areas of abnormal change in brain structure. This is the kind of damage that might occur with a sharply defined traumatic injury or an interruption of blood supply (a stroke) to a specific part of the brain
ischemic vs hemorrhagic stroke
Ischemic stroke
Cause: A blood clot or plaque buildup blocks blood flow to the brain
Symptoms: Weakness or numbness on one side of the body or face, difficulty speaking, vision or balance problems
Treatment: Thrombolytic drugs, blood thinners, or clot removal surgery
Hemorrhagic stroke
Cause: A blood vessel in the brain bursts, leaking or rupturing
Symptoms: Sudden headache, confusion, weakness or numbness on one side of the body
Treatment: Endovascular procedures, surgical treatment, medications to lower blood pressure
Diagnosis
left vs right hemipshere functions
functions that are dependent on serial processing of familiar information, such as language and solving mathematical equations, take place mostly in the left hemisphere for nearly everyone. Conversely, the right hemisphere appears to be generally specialized for grasping overall meanings in novel situations; reasoning on a nonverbal, intuitive level; and appreciating spatial relations. Even within hemispheres, the various lobes and regions mediate specialized functions
Damage to the frontal areas and symptoms
1) being unmotivated and passive and with limited thoughts and ideas or (2) featuring impulsiveness and distractibility.
parietal vs temporal lobe damage
amage to specific areas of the right parietal lobe may produce impairment of visual-motor coordination, and damage to the left parietal area may impair certain aspects of language function, including reading and writing, as well as arithmetical abilities. Damage to certain structures within the temporal lobes disrupts an early stage of memory storage. Extensive bilateral temporal damage can produce a syndrome in which remote memory remains relatively intact but nothing new can be stored for later retrieval. Damage to other structures within the temporal lobes is associated with disturbances of eating, sexuality, and emotion
occipital lobe damage
Occipital damage produces a variety of visual impairments and visual association deficits, the nature of the deficit depending on the particular site of the lesion.
Delirium
Delirium is a state of acute brain failure that lies between normal wakefulness and stupor or coma (see Figure 14.3). The word comes from the Latin delirare, meaning “to be out of one’s furrow or track.”
- characterized by confusion, disturbed concentration, and cognitive dysfunction (see the DSM-5 box for diagnostic criteria). Although the DSM-IV-TR criteria stated that delirium involved a disturbance in consciousness, the word consciousness was removed in DSM-5. This is because the essence of delirium is better captured by the idea of a disturbance in awareness. Think of delirium as a condition with a sudden onset that involves a fluctuating state of reduced awareness. Delirium is treated as a distinct disorder in DSM-5 (rather than as a type of major or mild neurocognitive disorder) because it can quickly fluctuate in severity. It can also coexist with a major or mild neurocognitive disorder (such as Alzheimer’s disease). It therefore does not fit well with being categorized as a major or mild form of neurocognitive disorder.
delirium and memory/hallucinations
delirium also involves impairments of memory and attention as well as disorganized thinking. Hallucinations and delusions are quite common (see Trzepacz et al., 2002). Moreover, the syndrome often includes abnormal psychomotor activity such as wild thrashing about and disturbance of the sleep cycle. A person who is delirious is essentially unable to carry out purposeful mental activity of any kind.
risk for delirium
Delirium can occur in a person of any age. However, the elderly are at particularly high risk, perhaps because of brain changes caused by normal aging that lead to reduced “brain reserve.” As described in the case of Mrs. Patterson, delirium is very common in the elderly after they have had surgery, with patients over age 80 being particularly at risk
-At the other end of the age spectrum, children are also at high risk of delirium, perhaps because their brains are not yet fully developed. In addition to advanced age, other risk factors for delirium include dementia, depression, and tobacco use (Fricchione et al., 2008). A reliable and easy screening test for delirium involves asking the patient to recite the months of the year backwards
delirium treatment
The medications that are used for most cases are neuroleptics (Fricchione et al., 2008; Lee et al., 2004). These are the same drugs that are used to treat schizophrenia. For delirium caused by alcohol or drug withdrawal, benzodiazepines (such as those used in the treatment of anxiety disorders) are used (Trzepacz et al., 2002). In addition, environmental manipulations that help patients stay oriented, such as good lighting, clear signage, and easily visible calendars and clocks, can be helpful. It is also important that staff members introduce themselves when they work with patients, explain what their role is, and provide reorienting prompts whenever necessary. Some patients, however, especially elderly ones, may still have orientation problems, sleep problems, and other difficulties even months after an episode of delirium.
Major Neurocognitive Disorder
Major neurocognitive disorders are those that involve marked deficits in cognitive abilities. These may be apparent in such areas as attention, executive ability, learning and memory, language, perception, and social cognition (skills required for understanding, interpreting, and responding to the behavior of others). What is crucial is that there is a decline from a previously attained level of functioning (see the DSM-5 table for diagnostic criteria for major neurocognitive disorder).
Treatable Causes of Major Neurocognitive Disorder
Medications
Clinical depression
Vitamin B12 deficiency
Chronic alcoholism
Certain tumors or infections of the brain
Blood clots pressing on the brain
Metabolic imbalances (including thyroid, kidney, or liver disorders)
Parkinson’s Disease
s the second most common neurodegenerative disorder (after Alzheimer’s disease). It is more often found in men than in women, and it affects between 0.5 and 1 percent of people between ages 65 and 69 and 1 to 3 percent of people over age 80
Parkinson’s disease is characterized by motor symptoms such as resting tremors or rigid movements. The underlying cause of this is loss of dopamine neurons in an area of the brain called the substantia nigra (located in the basal ganglia). Dopamine is a neurotransmitter that is involved in the control of movement. When dopamine neurons are lost, a person is unable to move in a controlled and fluid manner. In addition to motor symptoms, Parkinson’s disease can involve psychological symptoms such as depression, anxiety, apathy, cognitive problems, and even hallucinations and delusions
The symptoms of Parkinson’s disease can be temporarily reduced by medications, such as pramipexole (Mirapex) or levodopa/carbidopa (Sinemet), that increase the availability of dopamine in the brain either directly or indirectly. However, once the medications wear off, the symptoms return. Another treatment approach that is now being tried is deep brain stimulation (described in
excercise and parkinsons
k, patients not only improved their general level of fitness but also showed gains in motor function,
Huntington’s Disease
The illness begins in midlife (the mean age of onset is around 40 years), and it affects men and women in equal numbers. Huntington’s disease is characterized by a chronic, progressive chorea (involuntary and irregular movements that flow randomly from one area of the body to another). However, subtle cognitive problems often predate the onset of motor symptoms by many years. These cognitive problems are no doubt due to the progressive loss of brain tissue (detectable with brain imaging) that occurs as much as a decade before the formal onset of the illness (Shoulson & Young, 2011). Patients eventually develop dementia, and death usually occurs within 10 to 20 years of first developing the illness. There are currently no effective treatments that can restore functioning or slow down the course of this terrible and relentless disorder.
cause of huntington
Huntington’s disease is caused by a single dominant gene (the Huntingtin gene) on chromosome 4. (This is not a typo. The name of the gene is not the same as the name of the disease.) This genetic mutation was discovered as a result of intense research on people living in villages around Lake Maracaibo in Venezuela, where this disease is extremely common (Marsh & Margolis, 2009). Because the Huntingtin gene is a dominant gene, anyone who has a parent with the disease has a 50 percent chance of developing the disease himself or herself.
diagnosis of alzheimers
The diagnosis of Alzheimer’s disease is made after a thorough clinical assessment of the patient. However, the diagnosis can only be truly confirmed after the patient’s death. This is because an autopsy must be performed to see the brain abnormalities that are such distinctive signs of this disease. In the living patient, the diagnosis is normally given only after all other potential causes of dementia are ruled out by medical and family history, physical examination, and laboratory tests.
alzheimers onset and symptoms
Alzheimer’s disease usually begins after about age 45 (Malaspina et al., 2002). Contrary to what many people believe, it is characterized by multiple cognitive deficits, not just problems with memory. There is a gradual declining course that involves slow mental deterioration. Figure 14.5 shows the performance of two men on a battery of cognitive tests repeated over a period of several years. Both men were of similar age and level of education, and both were initially free of Alzheimer’s disease. However, for the man who subsequently developed Alzheimer’s disease (confirmed on autopsy), a progressive, downward course in his cognitive performance is apparent
=In its earliest stages, Alzheimer’s disease involves minor cognitive impairment. For example, the person may have difficulty recalling recent events, make more errors at work, or take longer to complete routine tasks. In the later stages, there is evidence of dementia; deficits become more severe, cover multiple domains, and result in an inability to function. For example, the person may be easily disoriented, have poor judgment, and neglect his or her personal hygiene. Because they have impaired memory for recent events, many patients have “empty” speech in which grammar and syntax remain intact, but vague and seemingly pointless expressions replace meaningful conversational exchange (
first brain regions to be damaged in alzheimers
The temporal lobes of the brain are the first regions to be damaged in the person with Alzheimer’s disease. Because the hippocampus is located here, memory impairment is an early symptom of the disease. Loss of brain tissue in the temporal lobes may also explain why delusions are found in some patients (Lyketsos et al., 2000). Although delusions of persecution are predominant, delusional jealousy is sometimes seen. Here, the person persistently accuses his or her partner or spouse—who is often of advanced age and physically debilitated—of being sexually unfaithful. Family members may be accused of poisoning the patient’s food or of plotting to steal the patient’s funds.
age and alzheimers
It has been estimated that the rate of Alzheimer’s disease doubles about every 5 years after a person reaches the age of 40 (Hendrie, 1998). Whereas fewer than 1 percent of 60- to 64-year-olds have the disease, up to 40 percent of those ages 85 and older
women seem to have a slightly higher risk of developing Alzheimer’s disease than men
Risk Factors for Alzheimer’s Disease
Advanced age
Female
Current smoker
Fewer years of education
Lower income
Lower occupational status
Head trauma
Obesity
Diabetes
alzheimers and location prevalence/why
The prevalence of Alzheimer’s disease is higher in North America and Western Europe and lower in such places as Africa, India, and Southeast Asia (Ballard et al., 2011; Ferri et al., 2005). Such observations have led researchers to suspect that lifestyle factors such as diet are implicated.
A Mediterranean diet consisting of a high intake of vegetables, fruit, nuts, and olive oil and a moderate intake of dairy, fish, poultry and meat seems to be beneficial for cognitive function (Ye et al., 2013). In contrast, obesity and having type 2 diabetes both increase the risk of developing Alzheimer’s disease (Christensen & Pike, 2015; Sridhar et al., 2015). The association with diabetes is especially interesting because researchers have found that insulin levels are abnormally low in some of the brain areas that are most affected by Alzheimer’s disease. A recent study has also demonstrated that cognitive function improves in people who are showing early signs of cognitive impairment when they are given insulin intranasally (so that it reaches the brain) for 21 days
microbiomes and alzheimers
! The role of these gut bacteria in a variety of diseases is now being explored. Remarkably, we are now learning that large amounts of amyloid (which, as you will shortly learn, is a sticky protein found in large amounts in the brains of patients with Alzheimer’s disease) are produced by microbes (Zhao & Lukiw, 2015). As of now, the significance of this is not clear. Because lines of inquiry involving diet and the gut microbiome are still at their earliest stages, we can say little that is definitive at present. Nonetheless, this is an exciting new research direction.
early-onset Alzheimer’s disease and APP gene
which account for only 1–2 percent of cases overall) appear to be caused by rare genetic mutations. So far, three such mutations have been identified (Guerreiro et al., 2012). One involves the APP (amyloid precursor protein) gene, which is located on chromosome 21. Mutations of the APP gene are associated with an onset of Alzheimer’s disease somewhere between 55 and 60 years of age (Cruts et al., 1998). Dominant mutations of this gene account for approximately 14 percent of early-onset cases
chromosome 21/down syndrome and alzheimers link
The fact that a mutation of a gene on chromosome 21 has been found to be important is interesting because it has long been known that people with Down syndrome (which is caused by a tripling, or trisomy, of chromosome 21) who survive beyond about age 40 develop an Alzheimer’s-like dementia
presenilin 1 (PS1) and very early onset alzheimers
Other cases of even earlier onset appear to be associated with mutations of a gene on chromosome 14 called presenilin 1 (PS1) and with a mutation of the presenilin 2 (PS2) gene on chromosome 1. These genes are associated with an onset of Alzheimer’s disease somewhere between 30 and 50 years of age (Cruts et al., 1998). One carrier of the PS1 mutation is even known to have developed the disorder at age 24 (Wisniewski et al., 1998). Remember, however, that these mutant genes, which are autosomal dominant genes and so nearly always cause disease in anyone who carries them, are extremely rare. The APP, PS1, and PS2 genetic mutations probably account, together, for no more than about 5 percent of cases of Alzheimer’s disease.
sporadic alzheimers
Most cases of Alzheimer’s disease are “sporadic,” meaning that they occur in patients without any family history, and develop later in life.
APOE (apolipoprotein) gene on chromosome 19 and late onset alzheimers
- This gene codes for a blood protein that helps carry cholesterol through the bloodstream. We know that differing forms (genetic alleles) of APOE differentially predict risk for late-onset Alzheimer’s disease. Three such alleles have been identified, and everyone inherits two of them, one from each parent. One of these alleles, the APOE-E4 allele, significantly enhances risk for late-onset disease. Thus, a person may inherit zero, one, or two of the APOE-E4 alleles, and his or her risk for Alzheimer’s disease increases correspondingly. For example, having one APOE-E4 allele increases risk by a factor of 3; having two APOE-E4 alleles results in an 8- to 10-fold increase in a person’s chances of developing the disease (Karch et al., 2014). Another such allele, APOE-E2, seems to convey protection against late-onset Alzheimer’s disease. The remaining and most common allele form (found in about 70 percent of the population) is APOE-E3, and is of neutral significance. The alleles differ in how efficient they are in clearing amyloid, with APOE-E2 being most efficient and APOE-E4 least efficient
APOE-E4 AND MEMORY DETEROIRATION
APOE-E4 has been shown to be a significant predictor of memory deterioration in older individuals with or without clinical dementia (Hofer et al., 2002). The APOE-E4 allele is relatively uncommon in Chinese people compared to its frequency in people from Europe or North America. In contrast, people of African descent are especially likely to have this allele
Genes Associated with Alzheimer’s Disease
Gene Chromosome Type
Amyloid precursor protein gene (APP) 21 Mutation
Presenilin 1 (PS1) 14 Mutation
Presenilin 2 (PS2) 1 Mutation
Apolipoprotein E (APOE) 19 Susceptibility gene
Depression AND Increases the Risk of Alzheimer’s Disease
Having a history of depression seems to put a person at higher risk for the later development of Alzheimer’s disease (Ownby et al., 2006). Although we are not yet sure why this is, researchers speculate that some of the changes in the brain that are known to be associated with depression and with stress may somehow leave the brain more vulnerable to problems down the road (Wilson et al., 2008).
Depression may also be an early warning sign of the onset of dementia.
Neuropathology FEATURES AND ALZHEIMERS
1) amyloid plaques, (2) neurofibrillary tangles, and (3) atrophy (shrinkage) of the brain.
amyloid plaques
neurons in the brain secrete a sticky protein substance called beta amyloid much faster than it can be broken down and cleared away. This beta amyloid then accumulates into amyloid plaques (see Figure 14.6). These are thought to interfere with synaptic functioning and to set off a cascade of events that leads to the death of brain cells. Beta amyloid has been shown to be neurotoxic (meaning it causes cell death). Amyloid plaques also trigger local chronic inflammation in the brain and release cytokines (see Chapter 5) that may further exacerbate this process. More generally, inflammation is now increasingly being viewed as a key factor, not only in the progression of Alzheimer’s disease but also in its development. The fact that many inflammatory processes are upregulated by obesity again highlights the link between lifestyle factors and Alzheimer’s disease.
why does amyloid plaque buildup happen
Having the APOE-E4 form of the APOE gene is associated with the more rapid buildup of amyloid in the brain (Jalbert et al., 2008). Animal studies also suggest that stress makes the neurocognitive consequences of amyloid accumulation much worse (Alberini, 2009; Srivareerat et al., 2009). Insulin may also play a role in regulating amyloid. (Again, this could help explain why diet and having diabetes have been identified as risk factors.) Although some scientists believe that the accumulation of beta amyloid plays a primary role in the development of Alzheimer’s disease, others suspect that it may be a defensive response rather than a causal factor. Importantly, amyloid deposits can be present as many as 10 years before clinical signs of Alzheimer’s disease first show themselves
Neurofibrillary tangles
e webs of abnormal filaments within a nerve cell. These filaments are made up of another protein called tau. In a normal, healthy brain, tau acts like scaffolding, supporting a tube inside neurons and allowing them to conduct nerve impulses. In Alzheimer’s disease the tau is misshaped and tangled. This causes the neuron tube to collapse.
Although abnormal tau aggregation can occur independently, there is reason to believe that buildup of tau protein is accelerated by an increasing burden of amyloid in the brain (Shim & Morris, 2011). Animal studies of mice that have been genetically modified to be highly susceptible to developing Alzheimer’s disease (so-called transgenic mice) support this idea
acetlycholine and alzheimers
Another notable alteration in Alzheimer’s disease concerns the neurotransmitter acetylcholine (ACh). This neurotransmitter is known to be important in the mediation of memory. Although there is widespread destruction of neurons in Alzheimer’s disease, particularly in the area of the hippocampus (Adler, 1994; Mori et al., 1997b), evidence suggests that among the earliest and most severely affected structures is a cluster of cell bodies located in the basal forebrain and involved in the release of ACh.
The loss of cells that produce ACh makes a bad situation much worse. Because ACh is so important in memory, its depletion contributes greatly to the cognitive and behavioral deficits that are characteristic of Alzheimer’s disease. For this reason, drugs (called cholinesterase inhibitors) that inhibit the breakdown of ACh (and so increase the availability of this neurotransmitter) can be clinically beneficial for patients
alzheimers treatment
- no treatment for Alzheimer’s disease that will restore functions once they have been destroyed or lost. Current treatments, targeting both patients and family members, aim to diminish agitation and aggression in patients and reduce distress in caregivers as much as possible
-Some common problematic behaviors associated with dementia are wandering off, incontinence, inappropriate sexual behavior, and inadequate self-care skills. These can be somewhat controlled via behavioral approaches (see Chapter 16). Behavioral treatments need not be dependent on complex cognitive and communication abilities (which tend to be lacking in patients with dementia)
-As we noted earlier, some patients with Alzheimer’s disease develop psychotic symptoms and become very agitated. Antipsychotic medications (like those used in the treatment of schizophrenia) are sometimes given to alleviate these symptoms. However, these medications must be used with great caution. The U.S. Food and Drug Administration has issued a warning that patients with dementia who receive atypical antipsychotic medications are at increased risk of death
-Currently, the most effective way of doing so is by inhibiting the production of acetylcholinesterase, the principal enzyme involved in the metabolic breakdown of acetylcholine.
-The newest medication that has been approved to treat Alzheimer’s disease is memantine, which is marketed as Namenda. Unlike other approved medications, memantine is not a cholinesterase inhibitor. Instead, it appears to regulate the activity of the neurotransmitter glutamate, perhaps by protecting cells against excess glutamate by partially blocking NMDA receptors. Memantine, which can be used alone or in combination with donepezil, appears to provide patients with some cognitive benefits
timing of damage to brain and alzheimers
Most researchers believe that damage to the brain begins long before (maybe a decade or more) clinical symptoms appear. To try and detect these toxic changes, researchers are using a range of brain-imaging techniques to study the brains of people at high risk for developing the disease. People at high risk include those who have the APOE-E4 allele as well as people who are experiencing minor cognitive impairment. MCI is thought to be on a continuum between healthy aging and the earliest signs of dementia
Cholinesterase-inhibiting medications
Cholinesterase-inhibiting medications are the mainstream treatment for Alzheimer’s disease, but they provide only limited benefits.
rTMS and tDCS alzheimer treatment
Researchers are now using noninvasive brain stimulation techniques such as repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) to try to improve cognitive functioning in patients with Alzheimer’s disease. rTMS changes brain activation through the delivery of strong magnetic pulses that pass through the scalp and to the cortex beneath. In tDCS, a weak electrical current is delivered to the scalp; the type of stimulation (anodal or cathodal) determines whether excitability in the underlying cortical areas is increased or decreased.
commonalities between MCI and alzheimer
Brain scans of people with MCI show that, like patients with Alzheimer’s disease, they have atrophy in a number of brain areas, including the hippocampus (which you may recall is involved in memory)
Functional imaging techniques also show that the hippocampus is less active when patients with Alzheimer’s disease (compared to controls) are engaged in memory tasks (Kato et al., 2001; Sperling et al., 2003). Again, this is also true of people with MCI
APOE-E4 and cognitive task performance among cognitively healthy
Current thinking is that the greater degree of brain activation in people who are cognitively normal but at high risk for developing Alzheimer’s disease reflects the greater effort they need to make to manage cognitive tasks. Simply put, carriers of the APOE-E4 allele may have to work harder. Because their brain tissue is still healthy (unlike in people with Alzheimer’s disease or MCI), we see an increase in brain activation in response to a cognitive challenge rather than the decrease in activation that is more typical of patients with Alzheimer’s disease or those with MCI. A similar pattern of increased brain activation in certain key areas is also found in people with MCI who are able to perform better on cognitive tests compared to those who perform worse
excercise and preserving brain function
If you want to preserve your brain function as you age, you may be surprised to learn that one of the best things you can do is to exercise regularly. A growing amount of research suggests that exercise has considerable neurocognitive benefits.
-exercise seemed to reverse the age-related loss, whereas stretching and toning did not. What is also interesting is that increases in the volume of the hippocampus were also directly related to improvements in memory
risks for caregivers
Not surprisingly, as a group, caregivers are at high risk for becoming socially isolated and for developing depression (Richards & Sweet, 2009). The stronger the bond they have with the person with Alzheimer’s disease, the more likely they are to become depressed and exhausted
vascular dementia
Neurocognitive disorder associated with vascular disease (vascular dementia) is frequently confused with Alzheimer’s disease because of its similar clinical picture of progressive dementia and its increasing incidence and prevalence rates with advancing age
circumscribed cerebral infarcts
circumscribed cerebral infarcts—interruptions of the blood supply to minute areas of the brain because of arterial disease, commonly known as “small strokes”—cumulatively destroy neurons over expanding brain regions. The affected regions become soft and may degenerate over time, leaving only cavities. Although vascular cognitive impairment tends to have a more varied early clinical picture than Alzheimer’s disease (Wallin & Blennow, 1993), the progressive loss of cells leads to brain atrophy and behavioral impairments that ultimately mimic those of Alzheimer’s disease
age onset of vascular cognitive impairement
Vascular cognitive impairment tends to occur after the age of 50 and affects more men than women (Askin-Edgar et al., 2002). Abnormalities of gait (e.g., being unsteady on one’s feet) may be an early predictor of this condition (Verghese et al., 2002). Vascular cognitive impairment is less common than Alzheimer’s disease, accounting for only 19 percent of dementia cases in a community sample of individuals age 65 years or older (Lyketsos et al., 2000). One reason for this is that these patients have a much shorter course of illness because they are vulnerable to sudden death from stroke or cardiovascular disease
amnestic disorder dsm 4 vs dsm 5
In DSM-IV-TR there was a specific and distinct diagnosis called amnestic disorder (amnestic is just another way of saying amnesia). In DSM-5, patients who would have been given this diagnosis are now diagnosed as having a major neurocognitive disorder. The cause of the disorder is also listed (e.g., major neurocognitive disorder due to substance use). Unlike other forms of neurocognitive disorder, however, the substantial decline in functioning occurs in a single cognitive domain (memory).
charachteristic features of amnestic disorders
The characteristic feature of neurocognitive disorders of this type (as shorthand we will still call them amnestic disorders) is strikingly disturbed memory. Immediate recall (i.e., the ability to repeat what has just been heard) is not usually affected. Memory for remote past events is also usually relatively preserved. However, short-term memory is typically so impaired that the person is unable to recall events that took place only a few minutes previously. To compensate, patients sometimes confabulate, making up events to fill in the void that they have in their memories.
. Korsakoff’s syndrome
is an amnestic disorder that is caused by a vitamin B1 (thiamine) deficiency. Because of this, the memory problems associated with Korsakoff’s syndrome can sometimes be reversed if the syndrome is detected very early and vitamin B1 is given. Korsakoff’s syndrome is often found in people with chronic alcoholism or in those who do not eat a healthy diet. It was the cause of the memory loss of the patient in the following case study.
causes of amnestic disorders
Another common cause of profound memory loss is head trauma. Stroke, surgery in the temporal lobe area of the brain, hypoxia (oxygen deprivation), and some forms of brain infections (such as encephalitis) can also lead to amnestic disorder. In these cases, depending on the nature and extent of damage to the affected neural structures and on the treatment undertaken, the disorder may remit with time. A wide range of techniques have been developed to assist the good-prognosis amnestic patient in remembering recent events (e.g., Gouvier et al., 1997). Moreover, because procedural memory (i.e., the ability to learn routines, skills, and actions) is often preserved in patients with amnesia, even patients without memory for specific personal experiences can still be taught to perform tasks that might help them reenter the workforce
Traumatic brain injury (TBI)
hildren ages 0 to 4, adolescents ages 15 to 19, and adults ages 65 years and older are most likely to experience a TBI. In every age group rates of TBI are higher for males than they are for females (Faul et al., 2010). In DSM-5 diagnostic terms such as major (or mild) neurocognitive disorder associated with head trauma are used to refer to the cognitive compromises that result from head injury.
People who play certain sports are at high risk of experiencing concussions and brain injuries. For males, the greatest risk comes from playing football; for females, the greatest risk comes from playing socce
tbi and explosives
In recent years there has been an escalation of cases of TBI in military personnel caused by explosive blasts (Champion et al., 2009). Blasts seem to damage the brain in ways that are different from the brain damage seen in civilian cases of TBI. So many veterans have been injured by improvised explosive devices that TBI has been referred to as the signature injury of the Iraq War. Research suggests that around 15 percent of soldiers who have served in Iraq have experienced a TBI (Hoge et al., 2008). The military has made many efforts to improve screening and to increase rehabilitation services for veterans (see Munsey, 2007). However, for many, a full recovery may never be possible.
clinical categorization of brain injuries
Clinicians categorize brain injuries as resulting from either a closed-head injury (where the cranium remains intact) or a penetrating head injury (where some object such as a bullet enters the brain). In closed-head injury, the damage to the brain is indirect—caused by inertial forces that cause the brain to come into violent contact with the interior skull wall or by rotational forces that twist the brain mass relative to the brain stem. Not uncommonly, closed-head injury also causes diffuse neuron damage because of the inertial force. In other words, the rapid movement of the rigid cranium is stopped on contact with an unyielding object. However, the softer brain tissue within keeps moving, and this has a shearing effect on nerve fibers and their synaptic interconnections.
retrograde vs antergorade amnesia
retrograde amnesia, or inability to recall events immediately preceding the injury. Apparently, the trauma interferes with the brain’s capacity to consolidate into long-term storage the events that were still being processed at the time of the trauma. Anterograde amnesia (also called posttraumatic amnesia) is the inability to store effectively in memory events that happen during variable periods of time after the trauma. (If you remember that anterograde and after both begin with an “a” you will remember this more easily.) Anterograde amnesia is also frequently observed and is regarded by many as a negative prognostic sign.
coma.
Following a severe injury and loss of consciousness, a person’s pulse, temperature, blood pressure, and important aspects of brain metabolism are all affected, and survival may be uncertain. In rare cases, an individual may live for extended periods of time without regaining consciousness, a condition known as coma. The duration of the coma is generally related to the severity of the injury. If the patient survives, coma may be followed by delirium, marked by acute excitement and disorientation and hallucinations. Gradually the confusion may clear up and the individual may regain contact with reality. Individual courses of recovery are highly variable and difficult to predict
Signs of a Concussion
Temporary loss of consciousness
Confusion or foggy feeling in the brain
Amnesia for the period surrounding the event/injury
Headache that gets worse and doesn’t go away
Nausea or vomiting
Excessive drowsiness
Slurred or incoherent speech
Difficulty remembering new information
Dizziness
These symptoms may not be immediately apparent.
Some symptoms may develop several days after the injury.
chronic postconcussion syndrome
(involving fatigue, irritability, memory loss, and depression)
chronic traumatic encephalopathy
CTE is a progressive form of brain damage involving neurodegeneration
APOE-E4 and post b rain injury problems
We are also learning something about the factors that may increase a person’s susceptibility to having problems after a brain injury. One important risk factor appears to be the presence of the APOE-E4 allele that we discussed earlier (Waters & Nicoll, 2005). In one study of boxers, the presence of the APOE-E4 genetic risk factor was associated with more chronic neurological deficits (Jordan et al., 1997). A study of patients being treated in a neurosurgical unit found that having the APOE-E4 allele risk factor predicted patients doing more poorly at a 6-month follow-up. This was true even after controlling for such factors as severity of the initial injury
gage
Brain injury can also result in changes in personality
A relatively common change is that the person becomes more easily emotionally dysregulated. This emotional lability is frequently accompanied by irritability or disinhibition. Less commonly, apathy and paranoia may also be apparent (Max et al., 2015). Personality changes have been reported in up to 40 percent of children with severe traumatic brain injuries. In a sample of adults who had experienced severe TBI, personality change was reported by their significant others in 59 percent of cases (Norup & Mortensen, 2015). The kinds of personality changes that emerge likely depend, in large measure, on the site and extent of the brain injury
children and tbis
Although one might think that children would fare better after a brain injury because of brain plasticity, this is usually not the case. Children who undergo significant TBI are more likely to be adversely affected the younger they are at the time of injury and the less language, fine motor, and other competencies they have. This is because brain damage makes it harder to learn new skills and because young children have fewer developed skills to begin with. Intellectual capacity, processing speed, attention, and memory are all affected. Social competence is also compromised. The severity of their injury, limited socioeconomic resources, and family dysfunction play a role in how well children recover (Catroppa et al., 2015; Karver et al., 2012; Rosema et al., 2012). The good news is that, when the injury is mild, most children emerge without lasting negative effects. Prospective longitudinal research also suggests that, although they may still have deficits, children who have experienced a significant TBI stabilize and can make appropriate developmental gains as they get older
