CHAPTER 14 Integrative Management of Disordered Cognition

OVERVIEW

Neurocognitive disorders (NCDs) are characterized by a significant decline in cognitive ability: These disorders are the most prevalent psychiatric disorders of late life, as the aging brain is sensitive and vulnerable to drugs, disease, and environmental factors.

complex attention, executive function, learning and memory, perceptual/motor function, and social cognition. As cognitive disorders include both acute onset (delirium) and gradual onset (major and mild NCDs), they may overlap or be difficult to diagnose.

complicated to comprehend and, thus, to assess and treat.

Age is usually considered to be an independent risk factor

incidence and prevalence of these impairments also are expected to increase.

CLASSIFICATION OF NEUROCOGNITIVE DISORDERS

cognitive changes associated with a major NCD are progressive and permanent, those associated with delirium are best assumed to be reversible, depending on the responsible causal factors. When the cause of delirium is eliminated or subsides, the cognitive deficits usually resolve within a few days or sometimes weeks. The NCDs, in contrast, result from primary brain pathology that usually is irreversible, progressive, and less amenable to disease-modifying treatment.

the assessment and management of these disorders, from mild cognitive impairment (MCI) to progressive chronic disorders, are similar.

GENERAL PRINCIPLES FOR ASSESSMENT OF OLDER ADULTS

Clients may not report symptoms and may endure debilitating symptoms and functional decline because they fear loss of independence or are embarrassed to report symptoms. Conditions that may contribute to cognitive impairments such as depression, alcoholism, and poor nutrition are commonly not reported, and nonspecific presentations such as fatigue, apathy, and poor concentration are typical. Even when reported, a cognitive change could signal depression, AD, an underlying urinary tract infection (UTI), or a myriad of other physical illnesses.

persons with AD will experience a clinically significant depression at some time in the course of the illness

an initial comprehensive biopsychosocial assessment is critical to detect and treat the condition. Aspects of a comprehensive assessment include physical, mental, functional, and social components, along with review of medications.

psychosocial as well as physical assessment. Follow-up after each episode of care to review the goals of treatment, evaluate progress toward remission of target symptoms, and prevent harm through careful assessment of medication use is a good practice.

detection of changes in cognition, mood, and functional status

increased risk for cognitive impairments due to rising rates of polypharmacy

Many drugs (medications, bioactive substances) affect the central nervous system (CNS), and normal age-associated changes in pharmacokinetics—including decreased total body water and bound drug, a change in the ratio of lean-to-fat distribution, diminished renal clearance and metabolism—can affect the pharmacodynamics properties of drugs and make clearance of drugs from the body unpredictable.

“brown bag method.” This involves asking the client and family to bring all prescription and nonprescription medications to the appointment. The PMH-APRN can then review and eliminate unneeded medications, teach the client about side effects and precautions, and possibly prevent an episode of delirium.

DELIRIUM

Delirium is characterized by a rapid onset of cognitive disturbance and altered consciousness induced by any process, disorder, or agent that disrupts the integrity of the CNS and impairs its functioning at a cellular level. The three hallmark diagnostic features of delirium are disordered cognition, impaired ability to maintain or shift attention, and disturbance of consciousness.

disrupted sleep–wake cycle and an abnormality of psychomotor behavior, either hyperactive or hypoactive. Hypoactive forms where the client presents as apathetic rather than agitated are often missed.

associated with significant mortality and morbidity both during and after hospitalization

preexisting cognitive impairments limiting capacity for self-care are at risk for delirium due to poor management of food and fluid intake, medications, and emerging illness.

treating and managing episodes of delirium resulting from urinary and upper respiratory infections (URIs), dehydration, and medication-related mishaps.

Assessment of Delirium

neuroinflammation, although the probable (cytokine) storm is likely silently started prodromal before the outward behavioral signs

identify clients who are vulnerable to the development of delirium, recognize early signs of delirium, determine the etiology, and rapidly institute measures to correct or reverse the underlying causes.

therapeutic goals include managing the acute confusion to prevent injury or further cognitive decline and education of the family or caregiver regarding the importance of prompt medical evaluation of any change in behavior.

hallmark characteristics of disordered attention and awareness

obtain information about the onset, duration, and course of the episode from a reliable informant who knows the client well, can describe changes from their normal baseline status, and can report any precipitating biopsychosocial stressors.

Ask about the hallmark symptoms of delirium: inability to focus attention, fluctuating consciousness, and disorganized thinking.

Laboratory evaluation - complete blood count (CBC), urinalysis, electrolytes, blood urea nitrogen, creatinine, glucose, thyroid function tests, and vitamin B12 and folate, along with a chest x-ray if there is evidence of URI and an EKG if there is evidence of heart disease.

assessing for syphilis (venereal disease research laboratory [VDRL test], rapid plasma reagin [RPR]), or heavy metal screening (lead, mercury, arsenic). Diagnostic scans such as CT or MRI -  recent head trauma, subdural hematoma, hydrocephalus, cerebral vasculitis, or tumor.

Screening Instruments for Delirium

Delirium Observation Screening (DOS) Scale

Confusion Assessment Method (CAM)

hallmark features of delirium: acute onset, fluctuating course, inattention, altered level of consciousness, and cognitive disorganization.

inpatient settings, the CAM has not been validated for use in outpatient settings

Outcomes

Outcomes will include resolution of the underlying cause of the delirium, ensuring safety of the client and caregiver, resolution of perceptual distortions, elimination of client anxiety, and restoration of the client to their previous level of cognitive and functional capacity.

Treatment of Delirium

Pharmacological Interventions

Medications should be minimized, used as a last resort, and triggered only by target symptoms such as severely agitated behavior, hallucinations, or paranoia severe enough to cause the client distress.

guidelines recommend avoiding the use of antipsychotics for management of delirium

Supportive Interventions

consult with the treatment team to ensure that they are aware of the client’s baseline functioning.

appropriate supportive measures that prevent risk of injury, iatrogenic illness due to medication administration, further disability, decline associated with immobility and use of restraints, and sensory deprivation or overload. Supportive measures focus on avoiding risk and increasing protective factors for the resolution of delirium. These include, but are not limited to, (a) close observation, (b) involvement of the family in care, (c) management of the environment to ensure adequate and appropriate levels of stimulation, (d) frequent reorientation of the client to the environment with explanation for all procedures, (e) ensuring adequate hydration and nutrition by offering fluids regularly, (f) establishment and implementation of a toileting schedule, (g) mobilization of the client to maintain conditioning, (h) utilization of comfort measures to decrease pain, and (i) client and family education regarding the transient and reversible nature of delirium to allay anxiety.

Prevention

Prevention of episodes of delirium is the best intervention. The PMH-APRN can practice primary, secondary, and tertiary prevention by (a) identifying and eliminating some of the risk factors associated with delirium by minimizing drug regimens and recommending influenza vaccines, (b) prompt recognition and treatment of conditions that may cause delirium, and (c) teaching caregivers of persons with cognitive impairment how to recognize acute changes in behavior as delirium and the importance of seeking prompt care to avoid further decline in functional status.

MILD NEUROCOGNITIVE DISORDERS

It is recognized that there are subtle and possibly normal cognitive changes associated with aging. For example, speed of processing, new learning, and retrieval and reaction time become potentially compromised with advancing age, but the impairments do not affect daily function and generally are not progressive.

preclinical stages of dementia, leading to a labeling of the disease as mild cognitive impairment (MCI).

MCI is defined as problems with memory or language severe enough to be noticeable to others or to be detected on cognitive tests, but not severe enough to interfere with activities of daily living (ADL). Scores between 26 and 30 on the Mini-Mental State Exam (MMSE) and less than 26 on the more sensitive Montreal Cognitive Assessment (MoCA) are indicative of MCI. If memory loss is the predominant feature, this is often referred to as amnestic MCI. As many as 20% of people over 65 years of age may have MCI: MCI may remain their diagnosis for many years or may progress to a major NCD; that is, MCI may be a latent major NCD.

MAJOR NEUROCOGNITIVE DISORDERS

several different types of NCDs, depending on etiology, all forms affect memory and cognition and are severe enough to impair normal function. Unlike delirium, consciousness is usually not affected until later stages.

primary or cortical types, of which AD is the prototype, and subcortical, of which vascular disease (VD) is the prototype. Further classification of NCDs due to infections, toxins, structural abnormalities, and other, possibly reversible

mild and major NCDs are described as well as the distinguishing features of AD, VD, Lewy body disease (LBD), Parkinson’s disease (PD), and substance use-related cognitive impairment.

every 5 years after age 65 the rate of AD doubles.

Etiology

sometimes be confirmed only upon postmortem examination, and can overlap, as in AD and VD. The risk factors include age, family history, genetics, cerebral VD, head trauma, and the presence of MCI. Persons with lower levels of education and lower socioeconomic status have higher rates of cognitive disease.

Extension of education may be protective due to developing more cognitive reserve, extending life, and limiting disability

Alzheimer’s Disease

AD is the most prevalent of the NCDs. It is a degenerative progressive neuropsychiatric disorder resulting in global impairment of cognition, emotions, and behavior leading to physical and functional decline and death. The precise etiology of AD is unknown and most likely multifactoral, a combination of genetic vulnerability and exposure to environmental and psychosocial stressors. The role of various biopsychosocial factors such as genetics, inflammation, oxidative stress, vascular changes, metabolic factors, beta-amyloid and tau proteins, lifestyles and education levels, hormones, and growth factors are being investigated.

The hallmark pathological features of AD are the presence of neurofibrillary tangles and beta-amyloid plaques in the brain on postmortem examination; the definitive diagnosis of AD is based on their presence. The disease process of AD results in neuronal death and the disruption of neurotransmission, especially that of the neurotransmitter acetylcholine (ACh), which is critically important to memory and cognition. Acetylcholinesterase inhibitors (ACIs) have demonstrated their efficacy in slowing the process of AD, and neuronal destruction with concomitant disruption of ACh transmission is thought to be a cause of cognitive impairment in AD.

genetic mutations on chromosomes 1, 14, and 21. People who carry the apolipoprotein E (apoE) gene found on chromosome 19 also carry higher risk for the disorder.

Damage to cells from oxygen-free radicals (oxidative stress) may cause neuron dysfunction resulting in the production of tangles, plaques, and cell death. Proinflammatory processes and high cholesterol levels have been investigated as a cause of AD. An immunological defect also has been implicated as a cause of AD because of abnormally high antibody titers found in some clients. A newer colloquial description for this complex iterative explanation is inflammaging.

exposure to environmental toxins, diet, lifestyle, and psychological stress

highly educated and have higher incomes have lower rates of AD. Education and participating in intellectually stimulating activities are thought to reduce risk.

Vascular Disease

VD results from multiple infarcts in the cortex and the white matter of the brain following brain hemorrhage or ischemia. It tends to appear comorbidly with AD rather than as a discrete entity.

most common dementia in men and in those older than 85 years. Risk factors for VD parallel those for cerebrovascular accident (CVA) and include hypertension, smoking, hyperlipidemia, atrial fibrillation, and diabetes. The course of VD has a more abrupt onset and stepwise pattern of progression

depends on the sectors of the brain affected and the extent to which they are damaged. Frequently, there is accompanying neurological evidence of cerebrovascular disease, such as paresis or paralysis of a limb or headaches. Diagnostic testing (MRI and CT scan)

On physical examination, the client may have carotid bruits, fundoscopic abnormalities, or enlarged heart chambers and focal neurological signs

Lewy Body Disease

characterized by earlier and more prominent visual hallucinations, parkinsonian features, behavior disturbances, and parasomnias

antipsychotic drugs are used to treat hallucinations, these clients often have significant adverse effects and worsening of agitated behaviors.

LBDs are the defining lesions found in the substantia nigra of persons with PD. These lesions are found in the limbic and cortical areas of the brain in a subgroup of individuals with late-onset dementia. The presence of Lewy inclusion bodies in the cerebral cortex on autopsy confirms the diagnosis. Because of some clinical similarity, LBD can be mistaken for AD.

Parkinson’s Disease

neurodegenerative illness characterized by a decreasing number of neurons in the substantia nigra, resulting in depletion of the neurotransmitter, dopamine

clinical picture is that of motor disturbance

resting tremor, slowness, and rigidity along with postural instability. The gait disturbance and cognitive deficits

does not impair the client’s language capabilities, as do many other NCDs, but it also does not spare the client’s memory retrieval and executive functioning.

Specialty care -neurologist

Because treatment with dopamine precursors and agonists to enhance movement may cause side effects appearing as hallucinations and delusions

Frontotemporal Lobar Degeneration

Frontotemporal lobar degeneration (FTLD), of which Pick’s disease is a subtype

Onset occurs between ages 40 years and 60 years, and men

cause is unknown, abnormal functions of tau protein (tauopathies) are associated with the illness and are being investigated as targets of treatment. In the beginning stages, the clients of this disorder have less disorientation and memory loss than those with AD, and more personality changes, including loss of social constraints, resulting in frequent behavioral problems. Apathy and lack of motivation

differentiate these behaviors from depression

A second type of FTLD, primary progressive aphasia, presents with aphasia rather than behavioral symptoms.

Other Forms of Neurocognitive Disorders

Huntington’s disease is a hereditary disorder caused by a faulty gene for a protein (huntingtin).

30s or 40s. As the course from onset to death is approximately 15 years

In untreated HIV/AIDS, the detection of major neurocognitive impairment is confounded by infections, tumors, and adverse reactions to drugs. The clinician should be alert for mild cognitive decline or neurological symptoms such as headaches, vision changes, and neuropathies that might signal CNS involvement in the client with AIDS. Symptoms may alternate between memory loss and confusion and mental clarity and can stabilize for months before resuming downward progression.

NCDs due to TBI may present in younger populations as a result of accidents and combat but is also a risk for older adults as a result of falls.

previous TBI were more than twice as likely to develop dementia. Symptoms of TBI can be mild, moderate, or severe, depending on the extent of the injury. Mild and subtle symptoms include physical symptoms such as headache, dizziness, and blurred vision, and neuropsychiatric symptoms such as difficulty with memory, attention, concentration, mood, and sleep. Although mild symptoms may appear to resolve, they can progress over years to measurable MCI and major cognitive disorders. Language and communication problems along with emotional and behavioral problems are typical with TBI.

Creutzfeldt–Jakob disease is a rare disease caused by a protein called a prion body that affects multiple neurological systems

Substance-Induced Major Cognitive Disorder—Amnestic Confabulatory Type

Amnestic disorders are characterized by short-term memory loss and decline in social and occupational functioning.

Korsakoff’s syndrome, one of the substance-induced persisting amnestic disorders, is most prevalent. A client with this disorder has great difficulty with recent, or episodic, memory, and therefore has difficulty learning new information. Because of the inability to recall recent events, the individual fills in memory gaps with fabricated or imagined data and stories can become quite fantastic. Wernicke’s syndrome describes the physical symptoms of ataxia, confusion, and paralysis of some of the motor muscles of the eye, whereas Korsakoff’s syndrome results from the lack of treatment at this stage. Both syndromes, Wernicke’s and Korsakoff’s, are caused by the client’s chronic alcohol use, resulting in poor nutritional intake and resulting thiamine deficiency that interferes with production of glucose in the brain. This syndrome is usually found in the 40- to 70-year-old client with a history of steady and progressive alcohol intake

COVID Considerations

diagnosis of NCD due to HIV Infection

potential infectious agents.

potentially lasting cognitive deficits

Delirium can be viewed both as an antecedent inflammatory process for post-COVID cognitive difficulty and as an independent risk factor for the development of dementia. Whether the cognitive deficits are the residual effect of a delirium which is often a marker of the coronavirus-related disease process or a separate mechanism of disease that is related to the transmission of the infection that crosses the blood–brain barrier.

ruling out potential other causes of acute confusion (i.e., delirium) and establishing if clients have MCI, a known precursor to a more progressive NCD.

CLINICAL SIGNS AND COURSE OF ALZHEIMER’S DISEASE (AS THE PROTOTYPE NEUROCOGNITIVE DISORDER)

The decline in intellectual ability and cognitive functional capacity seen in AD occurs for a 2- to 10-year period. Subtle changes in recent memory and personality occur early and may go unrecognized by all but the individual. As this prodromal phase ends, memory impairment becomes more severe and deficits in visuospatial and executive function appear. Difficulty finding words (aphasia) and performing tasks (apraxia) worsens. Eventually, the client experiences agnosia, the failure to recognize objects and people.

Staging also informs choice of interventions and assists clients and families to know where they are in the process of the illness

Though the diagnosis of NCD is based on both cognitive and functional capacity, MCI is now included as a first stage by some and biomarkers that can identify preclinical disease have been identified and are beginning to be used in clinical practice.

Amnestic MCI, described previously, is likely a latent, prodromal stage of dementia. At this stage, the client may temporarily forget where he placed an item, may forget names, and may find the word he was about to utter slipping away.

Early Stage

Early cognitive disorders are characterized by impaired short-term memory and inability to learn new material. Individuals may forget where they put something and repeat the same questions. Word finding becomes difficult and the client may attempt to compensate by describing the item when the name cannot be located. Complex tasks that were once easy for the client

become impossible. Changes in affect, behavior, and judgment are typical. Social skills are initially preserved but irritability and defensiveness may occur if the memory impairment is noted and addressed. Compensation for deficits

Apraxia, disorders of skilled movement, becomes evident at this stage. Ideomotor apraxia is the difficulty of translating an idea into the corresponding action, resulting in impairments in managing routine tasks and creating safety risks.

Intermediate Stage

In this stage, the client’s ability to learn new material and perform ADL declines as the client develops agnosia, or failure to recognize items, which may lead to misperception of the environment and further risk of injury. Significant agitation due to paranoid ideation, wandering, hoarding, and inappropriate sexual behavior often begin in this stage.

Behavior and affect may worsen over the course of the day, with more impairment toward evening.

Late Stage

In later stages, the individual will require total ADL assistance, will be unable to recognize even close family members, and will eventually develop dysphasia. The risk for dehydration and malnutrition is high along with infection, a typical cause of death in those affected.

Shared Decision-Making/Achieving Concordance

People who are living with dementia (PWD)

a person may not be suffering in the least, but the family care partners may experience suffering related to the person’s behavior or function that is out of the scope of the person with dementia’s awareness and insight.

early recognition and treatment to preserve function and help the client and family plan for the future

Recognition of those conditions that are reversible can restore cognition in some, and early diagnosis of AD can assist the client and family to secure resources, receive treatment, and preserve function as long as possible.

The four components of the approach to decision-making are Kickstart, Assess, Evaluate, and Refer (KAER), and the framework can be useful to recognize the strengths and needs of the client and their support network

Simple, clear information, use of visual aids, and allowing ample time to discuss options and ask questions will enhance communication and the therapeutic alliance. Discussion of the benefits as well as the limitations and side effects of medications will assist the client and family in making informed decisions regarding treatment options.

emotionally supportive milieu and focus on interventions that can improve quality of life and preserve function despite the inevitable trajectory of the illness.

Clients are often very anxious, may be suspicious, and are concerned about loss of independence.

In middle to later stages of cognitive impairment, it is important to continue efforts to communicate directly with the client through attentive listening, providing reassuring verbal and nonverbal cues, and observing nonverbal behaviors of the client that signal comfort or distress.

Information regarding the illness, the expected course, treatment, and intervention options, along with community resources and referrals to the Alzheimer’s Association

the client is the primary focus of assessment and intervention, family-centered care is critical to quality treatment outcomes.

assess caregivers for depression and anxiety as well as the identified client.

caregiver self-assessment instruments measuring strain, quality of life, and needs

The family or kin caregiver is the essential member of any healthcare team.

interventions such as individual supportive psychotherapy, cognitive behavioral therapy, respite care, day care, and others have shown some meaningful effects on reducing caregiver burden and depressive symptoms. The Alzheimer’s Association is one of the best resources for providing psychoeducational interventions

Assessment

history, the clinician needs to ask questions designed to assess the major symptoms of AD, including memory (the ability to learn and retain new information), cognition (handling complex tasks, reasoning ability, orientation, and language), and behavior. Specifically, questions designed to assess the neurocognitive domains of complex attention, executive function, learning and memory, language, perceptual motor, and social cognition

determining the presence of a cognitive disorder, a comprehensive history, physical examination, and diagnostic laboratory tests are necessary. The physical examination should include a neurological examination and a mental state examination with a formal assessment of cognition and memory.

DSM-5 criteria for determining AD include the presence of gradual, progressive, and insidious cognitive decline; impairment in memory and at least one other cognitive domain; and impairment in social and occupational functioning. The cognitive decline may include aphasia, apraxia, and/or agnosia in addition to decline in memory and executive functioning (planning, organizing, and sequencing).

History

assess and document symptoms related to the disorder and to ask about onset, duration, and progression

Physical

The client may attempt to hide symptoms, fearing that detection of the cognitive disorder may result in loss of independence or embarrassment. In the early stages, the client preserves social skills and is frequently able to appear intact. They may make up responses on the MMSE rather than appear impaired. A careful physical examination, including neurological assessment, may reveal reversible causes of cognitive impairment, detect impending delirium, differentiate VD, and aid in early detection of primary progressive cognitive disease.

Basic diagnostics - B12 and folate, serology, and CT or MRI scan

more comprehensive neuropsychiatric evaluation, PET, or single photon emission computed tomography (SPECT) scan.

Mental Status Examination

part of the physical examination

thought content and process, mood and affect, speech, perception, judgment and insight, and cognition and memory. In clients with disordered cognition

focused on the components of cognition including attention, memory, language and speech, visuospatial skills, and executive functioning.

Thought Content and Thought Process

Thought content (the “what” the person is thinking) and thought process (the “how” the person is thinking) is usually assessed through the proxy of what the person says, or through observation of behavior. Assessing thought process, such as loose associations, relies on an interaction with the client and assessment of their speech. Assessing thought content may require the assistance of a family member or other proxy to describe suspicious ideas or ideas of reference.

Mood and Affect

depression is prevalent, particularly in early stages of cognitive disorder. Older adults with undiagnosed depression frequently report problems with memory and concentration. Treatment of depression leads to improved functional capacity in clients with NCD and resolution of memory impairments in those who suffer from depression. As older adults have the highest rates of completed suicides

later stages of the disease, it is sometimes difficult to distinguish depressed affect from apathy associated with the disease progression. Therefore, asking about mood, observing affect, and asking the family about behavior

Geriatric Depression Scale (GDS)

pression are valuable clinical tools to both detect depression and track treatment response

rarer form of NCD may present with a euphoric or labile affect and an expansive or irritable mood.

Perceptual Distortions

including delusions and hallucinations, are a common feature

LBD, benign hallucinations

hallucinations, paranoia, accusatory behavior, and delusions

symptoms occurring in the moderate stage of dementia

The psychotic cluster of symptoms may lead to behavioral symptoms such as agitation and aggression, wandering, and screaming.

Judgment and Insight

context of cognitive evaluation along with the client’s history, general presentation, and demeanor. The MSE standard question, “What would you do if you found a stamped addressed envelope on the ground?” can reveal errors in judgment.

cognitive impairment may report having no idea why they are coming to the appointment

irritated with the family for expressing concern.

may believe they are competent to continue to drive or perform other activities that are no longer safe.

Cognition and Memory

open the interview by asking a question to assess abstract thinking such as “Tell me what you enjoy doing in your spare time.” If the response is abstract and well formed, no further formal assessment is indicated. If it is vague, without detail, or not concrete, further evaluation is warranted.

four subtypes of memory: episodic (related to personal experiences such as what one ate for breakfast), semantic (related to facts such as who is the president of the country), procedural (such as remembering how to drive), and working (the capacity to briefly retain information such as dialing a phone number

rapid cognitive screening of learning can be assessed by asking the client to repeat and remember three words. Working memory or calculation is assessed by asking him to state how much money he would have by adding a penny, a nickel, a dime, and a quarter. Semantic memory as well as language comprehension can be evaluated by naming the parts of clothing (e.g., lapel, collar, sleeve) as the examiner points to them. Finally, some aspects of procedural memory, ideomotor praxis, and temporoparietal function can be evaluated by asking the client to demonstrate opening a door with a key, slicing bread, using their left hand to point to the examiner's left hand, and giving a two-stage command such as “Before pointing to the ceiling, point to the door.” The clock draw test (CDT) is described later and is used to assess both visuospatial and executive functions. If the client does not do well on two or more of these measures, further evaluation with a standardized measure of cognition such as the MMSE, MoCA, diagnostic lab work, a neurological examination, or imaging is required.

Diagnostic Tools

Cognitive Screening Tools

Screening tools that assess cognition, mental state, and memory can assist the PMH-APRN in diagnosis as well as monitoring the effectiveness of interventions.

primary care include the Short, Portable Mental Status Questionnaire (SPMSQ), Folstein MMSE, CDT, the Mini-Cog Test, and the MoCA.

MMSE- standard for the assessment of memory. detecting and tracking progressive cognitive impairment. Scores less than 23 were initially recommended for sensitivity and specificity for dementia, but in highly educated populations, scores between 24 and 27 should trigger further evaluation.

MMSE-2 -  more sensitive to MCI

The SPMSQ was developed for use in primary care. It is a 10-item screening tool asking the client the date, month, and year; the day of the week; the name of the place; the client’s phone number; the client’s age and date of birth; the name of the current president; the president before the current president; and the client’s mother’s maiden name. The client is then asked to count backward from 20 by threes. A score of less than 2 indicates normal mental functioning; 3 to 4 errors, MCI; 5 to 7 errors, moderate cognitive impairment; and more than 8, severe cognitive impairment.

MMSE nor the SPMSQ assesses abstract thinking and frontal executive function, the PMH-APRN can add the CDT

Mini Cog or the MoCA. For the CDT, the client is asked to draw a clock, put the numbers on it, and place the hands at 20 after 8, or 10 after 11. This simple assessment tool tests executive functioning, visuospatial skills, and general organization. 3-point system allotting 1 point for the drawing, 1 for the numbers in the correct position, and 1 for the time depicted correctly.

Mini-Cog adds a three-word recall test to the CDT and is a good brief instrument. 3 minutes to draw the clock. If the client is unable to remember any of the three words after performing the CDT or draws the clock incorrectly, cognition is impaired. only in detecting the presence or absence of cognitive impairment but not for rating severity or monitoring progression of the disease. If cognition is impaired, the MMSE should be administered.

Another brief assessment measure is to ask the client to name as many animals as possible in a 1-minute span of time and each answer is scored 1 point. Scores less than 12 are abnormal and correlate well with scores less than 23 on the MMSE.

MoCA- tool to detect MCI and assess attention and concentration, executive functions, memory, language, visuospatial skills, abstract thinking calculations, and orientation. Visuospatial domains are assessed by asking the client to follow a numbered and lettered trail sequence and copy a cube. The CDT is used for executive function. Recognition is tested by asking the client to name three animals pictured. Memory is assessed by repeating a list of five words twice and asking the client to repeat them and then to recall them after 5 minutes. Repetition of five numbers forward and three backward, tapping at each A in a list of letters, and counting backward from 100 by sevens five times (serial sevens) tests for attention. Language is assessed by repeating two sentences and naming the maximum number of words beginning with the letter F. Asking the similarity between an orange and a banana, a train and a bicycle, and a watch and a ruler assesses the ability to think abstractly. Finally, orientation is assessed by asking the date, month, year, day, place, and city. The total score is 30; scores less than 26 indicate the presence of cognitive impairment

Functional Assessment Screening Tools

The FAQ is a 10-point list of functional activities completed by the informant rather than the client. The lower the score, the more impaired the client.

Physical ADL can be assessed using the Physical Self-Maintenance Scale (PSMS)

These rank physical ADL, including ability to bathe, dress, toilet, transfer, and feed oneself, along with continence. The PSMS asks the caregiver to rank client ability to perform toileting, feeding, dressing, grooming, physical ambulation, and bathing on a 1 to 5 scale, with 1 being independent and 5 totally dependent on others for care.

Dementia Rating/Staging Tools

Determining the stage and severity of AD

determining interventions, both pharmacological and nonpharmacological, in tracking progression of the disease, and in assisting and educating clients and caregivers. For example, selection of pharmacological agents is approved for different levels of disease severity and use of cholinesterase inhibitors (ChEIs) is not recommended once dementia is severe, as ACh is no longer being produced in sufficient quantity to warrant this intervention.

The four most commonly used instruments to rate and stage NCDs are the Functional Assessment Staging Test (FAST); the Global Deterioration Scale; the Clinical Dementia Rating (CDR) Scale; and the Blessed Dementia Rating Scale (BDRS).

The FAST is a seven-stage scale based on client function and correlating in earlier stages to MMSE scores.

The BDRS is a 22-item scale that assesses instrumental and physical ADL, along with behavior. It is completed by a reliable informant

The CDR is a rating of six domains: memory, orientation, judgment and problem-solving, community affairs, home and hobbies, and personal care.

Differential Diagnosis

mixed states are common

Detecting causes of cognitive decline such as that associated with major depressive disorder and delirium is the most critical component of assessment for the PMH-APRN. Depression that initially presents with difficulty concentrating or poor memory may be misdiagnosed as a NCD.

Delirium can be differentiated from a primary progressive NCD and depression by acute onset, the coexistence of another medical condition, memory disturbance of short duration, and rapid decline in functioning, along with the hallmark symptoms of impaired cognition, fluctuating consciousness, and inability to shift or maintain attention.

Expected Outcomes

overall treatment and management are aimed at improving the quality of life of the client and caregiver

treatment of the cognitive disorder and treatment of behavioral and psychological symptoms of dementia with both psychopharmacological and nonpharmacological measures.

DIFFERENTIAL DIAGNOSIS OF COMMON CONDITIONS PRESENTING WITH COGNITIVE IMPAIRMENTS

Delirium: Rapid (hours to days)/fluctuating

-Fluctuating level of consciousness, disorientation

Neurocognitive disorder, Alzheimer’s disease: Insidious onset/gradual progression

-Global cognitive impairment with memory deficits

Neurocognitive disorder, vascular disease: May be rapid, immediately following vascular incident such as cerebrovascular accident (CVA) or transient ischemic attack (TIA)

-Stepwise progression

-Stepwise deterioration in cognition and memory coincident with vascular events

Neurocognitive disorder, Lewy body disease:Insidious onset/fluctuating progression

-Parkinson features with gait disturbance; visual hallucinations, rapid eye movement (REM) sleep disturbance; sensitivity to neuroleptics

Neurocognitive disorder, frontotemporal lobar degeneration: Insidious onset/gradual progression

-Early personality change; problems with executive function; may be speech impairments; grasp and pout reflexes

Depression: Usually gradual. Differentiates from bereavement, which has sudden onset

-Sleep disturbance, appetite changes, weight loss or gain, anhedonia, sadness, feeling of worthlessness, guilt, somatic focus, hopelessness, helplessness

Sleep disorders: Variable depending on the cause

-Difficulty initiating and maintaining sleep, daytime sleepiness, disruption in daytime function

Substance abuse: Generally gradual

-Substance use out of control, affecting the ability to function; unexplained falls, episodes of confusion, and withdrawal symptoms; significant amnestic symptoms in late stages of chronic alcohol use

NONPHARMACOLOGICAL INTERVENTIONS FOR THE TREATMENT OF COGNITIVE IMPAIRMENTS

              Psychotherapy

              Somatic

              Complementary/alternative interventions

Avoid anticholinergic and limit psychotropic medications.

Treatment

Initiating Treatment to Preserve Cognitive and Functional Status

Initiation of treatment for neurocognitive disease requires consideration of the stage of the illness and the degree of functional capacity.

Active management through all the stages significantly improves quality of life, helps preserve function, and enhances coordination of care and use of resources

vigilant and forthcoming about expected symptoms at each stage of impairment and proactive regarding treatment options.

allowing time for processing and focusing on preservation of strength and function, rather than disability.

specialist such as a neurologist, geriatrician, or psychiatrist if the diagnosis is complex or unclear

identify the presence and severity of symptoms and prepare the client and family for subsequent visits that will occur two to three times a year or as needed to monitor cognitive and behavioral symptoms over the course of the illness. On each visit, assessment of safety concerns is crucial. Such issues as the client’s risk for wandering, agitation resulting in harm to self or the client’s caregiver, falls, self-harm accidents or suicidal ideation, and the adequacy of the support system should be addressed. assists the family to ensure appropriate levels of supervision for ADL based on the stage of functional and cognitive decline

Initiating Treatment to Manage Behavioral or Mood Disturbances

may require additional guidance on how to manage behavioral disturbances and psychotic symptoms that may emerge.

Psychotherapeutic and Nonpharmacological Interventions

Psychotherapy for people with dementia is founded on the assumption that wellness, function, and dignity are to be preserved and supported through the life span of the person.

benefit of interpersonal, here-and-now therapeutic encounters; and reminiscence therapy and person-centered therapy have continuing merit. Individual psychotherapy  for a person who is experiencing early onset of cognitive dysfunction may focus on the person’s goals and hopes (a strengths-based approach) or may address worry, uncertainty, loss, and powerlessness.

encouraged to stay cognitively, socially, and physically active, and emotionally engaged, and to follow a heart-healthy diet along with management of cardiac risk factors.

Cognition-oriented treatments including reality orientation, cognitive retraining, and skills training have been associated with slight cognitive gains.

Stimulation-oriented treatments include activities that have been shown to improve mood, cognition, and function, such as music, crafts, games, gardening, and cooking. Occupational therapy programs focusing on activity and socialization and day treatment programs have demonstrated benefits to cognitive function.

early stages of the disease -appointment book or personal data assistant (PDA), establishing a routine, keeping activities manageable, and engaging in stimulating, enjoyable, and stress-free activity to help preserve function. Stimulating memory, cueing, and reinforcement of attempts to fully engage in ADL performance are helpful.  short-term improvements in memory include cognitive behavioral approaches, reminiscence therapy, and supportive psychotherapy.

Physical activity has been associated with improvements in cognition and function and should be recommended for all persons with NCDs

Difficult behaviors such as wandering and agitation, screaming, and acute confusion at sundown often emerge in the moderate stages of disease. Symptoms of psychosis such as delusions and hallucinations are typical of this stage as well. Behavior-oriented treatments that focus on recognition of triggers for problem behaviors and modification of the environment to eliminate them are helpful, as are caregiver education and support, activity programs, music, and light therapy. comprehension is often better than expression, so attempts to maintain communication should be encouraged although the caregiver may become frustrated with repetitive questions and accusations based on delusions.

avoiding changes in routine, ensuring the client has daily activity and physical exercise, using distraction, and avoiding arguments.

Safety measures such as disconnecting the stove, placing locks on doors, and wearing safe-return bracelets need to be in place by this stage

Middle stage dementia is when care is often provided at home in the community, so home-based interventions could reduce dependence and increase engagement of the person, as well as improve the well-being and confidence of the caregiver

emergence of behavioral symptoms that client needs often begin to outstrip caregiver resources, financial, physical, and emotional. Transition to long-term care often begins at this point in the illness trajectory.

In the final, severe stage of disease, the client is totally dependent on others and requires nursing care.

Complementary and Integrative Interventions for Clients and Caregivers

Complementary and integrative interventions can offer stress relief and the prospect of improved ability to cope and better quality of life for caregivers and lessening of catastrophic reactions for clients. Interventions such as meditation, yoga, relaxation breathing, progressive relaxation, Tai Chi.

two broad major classifications of complementary health interventions: natural practices and mind–body interventions.

Natural products include the use of herbal and other supplements. Mind–body interventions include relaxation therapy, meditation, biofeedback, hypnosis, and imagery as well as manipulative body-based methods such as chiropractic, acupuncture, and massage therapy. Other modalities include movement therapies such as Tai Chi, Feldenkrais, Alexander techniques, and Pilates; the manipulation of energy fields including the use of magnet therapy, light therapy, and healing touch; and the use of traditional healers and spiritually based practices such as chanting and prayer.

A number of herbals, supplements, and dietary foods including ginkgo biloba, coenzyme Q10, vitamin B supplements, omega-3 fatty acids, and others have been promoted as memory enhancers

Some foods such as blueberries, deep water fish, and turmeric are thought to have antioxidant properties that support health and preserve cognition.

cardioprotective is thought to be neuroprotective.

informed about the anticoagulant effects of ginkgo and to be cautioned to observe for bleeding if used with other anticoagulants.

omega-3 fatty acids have been demonstrated to have a positive effect on cognition, most likely because of their antioxidant properties and effects on the heart, blood vessels, and nerve membranes.

Stress and resulting sympathetic release of cortisol is known to reduce cognition and further compromise functioning.

demonstrated to reduce stress in clients and improve coping and self-efficacy in caregivers. Similarly, yoga and Tai Chi have not been found to improve cognition but have been very effective in reducing stress and agitated behaviors and improving strength, balance, and general well-being. The use of massage therapy has demonstrated effectiveness in enhancing well-being and reducing anxiety, pain, and agitation.

Other modalities such as movement and exercise, bright light, and music have been effective in managing agitated behaviors and improving sleep. Multisensory environments known as Snoezelen rooms that incorporate music, aromatherapy, appealing nature sounds, and visual images of sunrises or starry skies have been found to diminish agitation and wandering.

Pharmacological Interventions

Pharmacological Treatment for Cognitive Symptoms

modifying or slowing a disease process.

ChEIs for clients in early-stage disease and some authors suggest use of these medications for amnestic MCI as well. The recommendations are based on the efficacy of the medications in slowing the cognitive decline and functional impairments associated with dementia. The neuropathological changes characteristic of AD lead to deficits in the enzyme that synthesizes ACh. Loss of cholinergic neurons and loss of ACh, which has an important role in learning and memory, led to the cholinergic hypothesis to account for the symptom pattern of memory loss in clients with AD. Thus, ChEIs were developed to counteract the effects of decreased ACh by preventing the destruction of ACh by the enzyme, acetylcholinesterase. The improvements in pharmacotherapy for dementia include simplification of dosing (e.g., to reduce the need for frequent dosing) and transdermal in addition to oral administration.

The three ChEIs are donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl or Razadyne). -slowing cognitive decline and in delaying transition to nursing home placement

rivastigmine and donepezil, which are in the same class, may be effective in treating cognitive symptoms. Donepezil (Aricept) can be given once a day beginning at 5 mg and titrated to 10 mg daily. Donepezil available in 23 mg daily formulation is only approved for use in moderate to severe stages of disease and is associated with increased side effects without significant increased benefit.

gastrointestinal (GI) side effects of the ChEI agents can be significant

dosing should begin at the lowest point for 1 month, and then be titrated up. The medications should be taken after eating. Ginger ale can help alleviate nausea and OTC preparations such as loperamide hydrochloride would be used cautiously for diarrhea

As the progression of dementia is slowed by an average of 2 years but is not stopped by the use of ChEI agents, memantine (Namenda) was developed and approved by the FDA as an agent for moderate to severe dementia. Therefore, it is used as a second-line agent to be added to ChEI agents when there is clinical and measurable change in cognition or functional status. Memantine is an N-methyl-D-aspartate (NMDA) glutamate receptor antagonist, which is thought to counteract the effect of excessive glutamate levels in the cortex of AD clients that may contribute to memory deficits. It has shown some benefits for clients with mild cognitive loss due to VD

Side effects are generally mild but may include dizziness, constipation, and headache. Some clients become too energized on the medication.

Lower dosing is also indicated if there is renal impairment.

A combination formulation of the ChEI drug donepezil with the NMDA drug memantine extended release (ER) was approved for treatment of persons in moderate to severe stages of disease. It is presumed that the person with AD will have been taking both donepezil and memantine prior to the initiation of the combination capsule.

Pharmacological Treatment of Mood, Psychosis, and Behavioral Symptoms

Depression is very prevalent in persons with disordered cognition, arising most likely from both the psychosocial and biological effects of the chronic debilitating illness. Persons with MCI or major cognitive disorder are likely to exhibit depression in the early to early-middle stages of the illness. An increase in irritability rather than clear dysphoria may indicate the presence of depression. Differentiation of depression from apathy can be challenging, but usually the person with apathy does not report poor mood.

treatment of depression - selective serotonin reuptake inhibitors (SSRIs) or serotonin–norepinephrine reuptake inhibitors (SNRIs). Citalopram (Celexa) is commonly used for clients with dementia due to its lower potential for side effects, and duloxetine (Cymbalta) is the agent of choice for the client who has neuropathic pain and depression. Treatment of depression will improve functional status and quality of life even if it has no direct effect on cognition

psychosis and agitation are common, particularly in the intermediate stages. Medications should be avoided and nonpharmacological interventions. assessment of behavior to detect occult pain, depression, sleep deprivation, or delirium.

If symptoms remain, assess and modify the environment, provide safety, and institute nonpharmacological measures.

If there are no other choices, identify target symptoms and institute drug therapy very cautiously. While second-generation antipsychotics—particularly quetiapine (Seroquel), risperidone (Risperdal), and olanzapine (Zyprexa)—have been used to manage hallucinations and agitation in persons with cognitive impairment, they all now have an FDA black box warning for use in older clients with dementia due to a heightened risk of death from cardiac events.

use of atypical antipsychotics as being associated with worsening cognition in persons with AD.

If the client has hypomanic or manic symptoms, initiate a mood stabilizer such as carbamazepine or divalproex, then add an atypical antipsychotic if needed. If there are psychotic symptoms, use an atypical antipsychotic in monotherapy. If there is agitation or aggression, choose an SSRI or mood stabilizer or trazodone. Trazodone is the treatment of choice for sleep disturbances. An SSRI is usually the treatment of choice for anxiety, a mood stabilizer for physical aggression or severe agitation, and trazodone for limited agitation associated with sun downing and for treatment of sleep disturbance. Benzodiazepines such as lorazepam (Ativan) must be used with caution for short-term management of anxiety and agitation due to the potential for falls, worsening of cognition, and further disinhibition. The presence of agitation may actually be a marker of an adverse drug reaction (i.e., of delirium).

obtaining baseline liver function and CBC testing prior to initiation of treatment with mood-stabilizing drugs.

Acute Follow-Up and Maintenance Treatment

Management of behavioral symptoms, acute confusion, physical illness, or sleep disturbances may require a more urgent visit.

neuropsychological assessment each year is indicated to detect changes in scores and initiate treatment early to slow further cognitive decline.

PEDIATRIC POINTERS

etiology such as trauma, tumors, infections, drugs and toxins, metabolic disturbance, and stress that affects adults can also cause disordered cognition in children.

Children may exhibit distress through behaviors such as withdrawal, anger, and poor performance at school.

Children and adolescents can be included in caregiving and can assist the client to stay socially, cognitively, emotionally, and physically engaged through activities

AGING ALERTS

screening of memory should be part of an annual wellness visit for all persons older than 65 to establish a baseline, promote cognitive health, and provide early detection and treatment of cognitive disorders.

screening for mood disorders should be part of annual wellness visits for elders to promote healthy aging, establish a baseline to detect changes, and treat depression. mental health and physical health are closely intertwined. Psychiatric illness, such as depression, may present as memory loss with difficulty concentrating and attending, and forms of dementia may initially appear with behavioral symptoms suggesting psychiatric illness.

Detection of depression in older adults is critical, as older adults, particularly those diagnosed with a chronic illness and those with a new diagnosis of a NCD, are at increased risk for suicide. Suicide is tragic and often preventable.

GDS or the Hamilton Depression Scale

screening for depression in older adults.

OVERVIEW

Neurocognitive disorders (NCDs), characterized by significant cognitive decline, are prevalent psychiatric disorders in late life due to the aging brain's sensitivity to drugs, disease, and environmental factors. They encompass various cognitive domains such as attention, executive function, memory, perceptual/motor function, and social cognition, and can present as either acute onset (delirium) or gradual onset (major and mild NCDs).

CLASSIFICATION OF NEUROCOGNITIVE DISORDERS

• Cognitive changes in major NCDs are progressive and permanent, while delirium may be reversible.

• Assessment and management are similar across the spectrum from mild cognitive impairment (MCI) to more severe disorders.

GENERAL PRINCIPLES FOR ASSESSMENT OF OLDER ADULTS

• Older adults often do not report symptoms due to fear of losing independence or embarrassment.

• Conditions like depression, alcoholism, and poor nutrition are often unreported contributors to cognitive impairments.

• Comprehensive assessment should include history of physical, mental, functional, and social factors, along with medication review.

DELIRIUM

• Delirium features rapid onset cognitive disturbances and altered consciousness, resulting from disruptions in the CNS.

• Hallmarks include disordered cognition, impaired attention ability, and altered level of consciousness.

• Management focuses on identifying and treating underlying causes and ensuring client safety.

Assessment of Delirium

• Key steps include identifying vulnerabilities, recognizing early signs, and determining the cause.

• Hallmark symptoms: inability to focus, fluctuating consciousness, disorganized thinking.

• Laboratory evaluations should include CBC, electrolytes, glucose, and possibly imaging studies.

MILD NEUROCOGNITIVE DISORDERS

• Mild cognitive impairment (MCI) is where cognitive problems are noticeable but do not interfere with daily living.

• Proposed threshold for MCI includes scores below 26 on the Montreal Cognitive Assessment (MoCA).

MAJOR NEUROCOGNITIVE DISORDERS

• Major NCDs impair normal function, affecting memory and cognition. They include various classifications based on etiology (AD, VD, LBD, PD).

• Risk factors for major NCDs include age, family history, and low education levels.

Alzheimer’s Disease (AD)

• Most prevalent NCD, resulting in global impairment of cognition and behavior. Hallmarks include neurofibrillary tangles and beta-amyloid plaques.

Vascular Disease (VD)

• Results from multiple brain infarcts related to ischemia or hemorrhage, exhibits a stepwise progression.

Lewy Body Disease (LBD)

• Notable for visual hallucinations and parkinsonian features, it complicates treatment due to sensitivity to antipsychotics.

Parkinson’s Disease (PD)

• Neurodegenerative disease primarily affecting movement but may also influence cognition.

Frontotemporal Lobar Degeneration (FTLD)

• Onset occurs between ages 40-60, characterized by personality changes and behavioral disturbances.

OTHER NEUROCOGNITIVE DISORDERS

• Examples include Huntington’s disease, traumatic brain injury (TBI)-related disorders, and substance-induced major cognitive disorders.

Assessment and Diagnosis

• Comprehensive history and mental status exams are critical.

• Differential diagnosis requires distinguishing between cognitive impairments from depression, delirium, or other medical conditions.

Outcomes and Treatment

• Treatment focuses on improving quality of life through pharmacological, psychotherapeutic, and supportive measures. Nonpharmacological interventions are emphasized, alongside careful management of medications.

KEY TAKEAWAYS

• Early detection and comprehensive assessments are vital for the management of neurocognitive disorders.

• Understanding the nuanced presentations of NCDs can improve diagnosis and care for affected individuals.