4th edition as of August 2026

 

Module Overview

In Module 14, we will cover matters related to neurocognitive disorders (NCDs) to include their clinical presentation, epidemiology, etiology, and treatment options. Our discussion will include delirium, major neurocognitive disorder, and mild neurocognitive disorder. We also discuss nine subtypes to include: Alzheimer’s disease, traumatic brain injury (TBI), vascular disorder, substance/medication induced, dementia with Lewy bodies, frontotemporal NCD, Parkinson’s disease, Huntington’s disease, and HIV infection. Be sure you refer Modules 1-3 for explanations of key terms (Module 1), an overview of the various models to explain psychopathology (Module 2), and descriptions of the therapies (Module 3).

 

Module Outline

• • 14.1. Clinical Presentation

• • 14.2. Epidemiology

• • 14.3. Etiology

• • 14.4. Treatment

 

Module Learning Outcomes

• Describe how neurocognitive disorders present.
• Describe the epidemiology of neurocognitive disorders.
• Describe the etiology of neurocognitive disorders.
• Describe treatment options for neurocognitive disorders.

 

---

14.1. Clinical Presentation

 

Section Learning Objectives

• Describe how delirium presents.
• Describe how major neurocognitive disorder presents.
• Describe how mild neurocognitive disorder presents.

 

Unlike many of the disorders we have discussed thus far, neurocognitive disorders often result from disease processes or medical conditions. Therefore, it is important that individuals presenting with these symptoms complete a medical assessment to better determine the etiology behind the disorder.

There are three main categories of neurocognitive disorders—delirium, major neurocognitive disorder, and mild neurocognitive disorder. Within major and minor neurocognitive disorders are several subtypes due to the etiology of the disorder. For this book, we will review diagnostic criteria for both major and minor neurocognitive disorders, followed by a brief description of the various disease subtypes in the etiology section.

It is important to note as well that the criteria for the various NCDs are based on defined cognitive domains. These include the following, with a brief explanation of what it is:

1. Complex attention – Sustained, divided, or selective attention and processing speed
2. Executive function – planning, decision-making, overriding habits, mental flexibility, and responding to feedback/error correction
3. Learning and memory – includes cued recall, immediate or long-term memory, and implicit learning
4. Language – Includes expressive language and receptive language
5. Perceptual-motor – Includes any abilities related to visual perception, gnosis, perceptual-motor praxis, or visuo-constructional
6. Social cognition – Includes recognition of emotions and theory of mind

 

14.1.1. Delirium

Delirium is characterized by a notable disturbance in attention along with reduced awareness of the environment. The disturbance develops over a short period of time, representing a change from baseline attention and awareness, and fluctuates in severity during the day. There is also a disturbance in cognitive performance that is significantly altered from one’s usual behavior. Disturbances in attention are often manifested as difficulty sustaining, shifting, or focusing attention. Additionally, an individual experiencing an episode of delirium will have a disruption in cognition, including confusion of where they are. Disorganized thinking, incoherent speech, and hallucinations and delusions may also be observed during periods of delirium.

Delirium is associated with increased functional decline and risk of being placed in an institution. That said, most people with delirium recover fully with or without treatment, especially if not elderly, but if undetected or the underlying cause is untreated, it may progress to stupor, coma, seizures, or death (APA, 2022).

 

14.1.2. Major Neurocognitive Disorder

Individuals with major neurocognitive disorder show a significant decline in both overall cognitive functioning (see the previously listed six domains) as well as the ability to independently meet the demands of daily living such as paying bills, taking medications, or caring for oneself (APA, 2022). While it is not necessary, it is helpful to have documentation of the cognitive decline via neuropsychological testing within a controlled, standardized testing environment. Information from close family members or caregivers is also important in documenting the decline and impairment in areas of functioning.

Within the umbrella of major neurocognitive disorder is dementia, a striking decline in cognition and self-help skills due to a neurocognitive disorder. The DSM-5-TR (APA, 2022) refrained from using this term in diagnostic categories as it is often used to describe the natural decline in degenerative dementias that affect older adults; whereas neurocognitive disorder is the preferred term used to describe conditions affecting younger individuals such as impairment due to traumatic brain injuries or other medical conditions. Therefore, while dementia is accurate in describing those experiencing major neurocognitive disorder due to age, it is not reflective of those experiencing neurocognitive issues secondary to an injury or illness.

 

14.1.3. Mild Neurocognitive Disorder

Individuals with mild neurocognitive disorder demonstrate a modest decline in one of the listed cognitive domains. The decline in functioning is not as extensive as that seen in major neurocognitive disorder, and the individual does not experience difficulty independently engaging in daily activities. However, they may require assistance or extra time to complete these tasks, particularly if the cognitive decline continues to progress.

It should be noted that the primary difference between major and mild neurocognitive disorder is the severity of the decline and independent functioning. Some argue that the two are earlier and later stages of the same disease process (Blaze, 2013). Conversely, individuals can go from major to mild neurocognitive disorder following recovery from a stroke or traumatic brain injury (Petersen, 2011). The DSM-5-TR describes major and mild NCD as existing on a spectrum of cognitive and functional impairment (APA, 2022, pg. 685).

 

 

 

---

14.2. Epidemiology

 

Section Learning Objectives

• Describe the epidemiology of neurocognitive disorders.

 

14.2.1. Delirium

The prevalence of delirium in the general community is relatively low at 1% to 2% based on data from the United States and Finland. For older individuals presenting to North American emergency departments, the rate is 8% to 17%. Results from the 2023 Cross-Sectional World Delirium Awareness Day Prevalence Study show that the prevalence of clinically documented delirium was 16.4% at 8:00 a.m. and 17.9% at 8:00 p.m. and significantly differed between age groups, reported discipline, unit, and hospital types (the researchers were primarily interested in the prevalence of clinically documented delirium at 8:00 a.m. and 8:00 p.m. on March 15, 2023; Lindroth et al., 2024). For those in nursing homes or post-acute care settings prevalence is 20 to 22% and 88% for individuals with terminal illnesses at the end of life. Wu et al. (2025) found that older age increased delirium risk but was mitigated the more years of education a person had. Prevalence rates are lower for younger African Americans compared to White individuals of similar age though Pan et al. (2025) found delirium risks to be higher among minoritized and socio-economically marginalized older adults and state that society should consider social marginalization as an important factor in delirium risk stratification.

 

14.2.2. Major and Mild NCD

Major and mild neurocognitive disorder prevalence rates vary widely depending on the etiological nature of the disorder and overall prevalence estimates are generally only available for older populations. It is estimated that 10% of people develop a neurocognitive disorder at some point in their life and unsurprisingly, it becomes more common with increasing age. For instance, an NCD occurs in 1-3% of individuals aged 65-74, 19% between 75 and 84, and up to 30% of individuals by age 85. After age 85 prevalence climbs to about 50%.

The female gender is associated with higher prevalence of major NCD overall, with more women being diagnosed with Alzheimer’s disease. The overall prevalence of mild NCD is similar across genders. In the U.S., incidence is highest in African Americans followed by American Indians/Alaska Natives, Latinx, Pacific Islanders, non-Latinx Whites, and Asian Americans. This trend is influenced by socioeconomic status, access to healthcare, and underlying health conditions (Wright et al., 2021).

 

14.2.3. Major and Mild NCD Subtypes

Alzheimer’s disease, the most commonly diagnosed neurocognitive disorder, is observed in nearly 5.5 million Americans (Alzheimer’s Association, 2017a), with 11% of those aged 65 and older and 32% older than 85 having dementia due to Alzheimer’s disease. It should also be noted that somewhere between 60-90% of dementias are attributable to Alzheimer’s disease, depending on the setting and diagnostic criteria. In terms of ethnoracial background in the U.S. the highest prevalence rates have been found among African Americans and Latinx of Caribbean origin (APA, 2022). Worldwide, 55 million people are living with Alzheimer’s and other dementias according to the Alzheimer’s Association (2026).

Over 2.87 million traumatic brain injuries (TBIs) happen each year within the United States, with men being 40% more likely to experience a TBI compared with women. The most common causes of TBI, in order of occurrence, are falls followed by collision with a moving or stationary object, automobile accidents, and assaults. It has also become increasingly recognized that concussion in sport causes mild TBI (APA, 2022).

 

1. What is the rate of occurrence of the neurocognitive disorders?

 

---

14.3. Etiology

 

Section Learning Objectives

• Define progressive.
• Describe the symptoms and causes of Alzheimer’s disease.
• Describe the symptoms and causes of traumatic brain injury (TBI).
• Describe the symptoms and causes of vascular disorders.
• Describe the symptoms and causes of substance/medication-induced major or mild NCD.
• Describe the symptoms and causes of dementia with Lewy bodies.
• Describe the symptoms and causes of frontotemporal NCD.
• Describe the symptoms and causes of Parkinson’s disease.
• Describe the symptoms and causes of Huntington’s disease.
• Describe the symptoms and causes of HIV infection.

 

Neurocognitive disorders occur due to a wide variety of medical conditions, neurological diseases, substance effects, or injuries to the brain. Therefore, this section will focus on a brief overview of the nine etiological categories of neurocognitive disorders per the DSM-5-TR (APA, 2022). As you will see, many of these neurocognitive disorders are both progressive, which means the symptoms worsen over time, as well as degenerative, which means neurons and/or brain structures deteriorate over time.

Per the DSM-5-TR (APA, 2022), an individual will meet diagnostic criteria for either mild or major neurocognitive disorder as listed above. In order to specify the type of neurocognitive disorder, additional diagnostic criteria specific to one of the following subtypes must be met.

 

14.3.1. Alzheimer’s Disease

Alzheimer’s disease is the most prevalent neurodegenerative disorder. While the primary symptom of Alzheimer’s disease is the gradual progression of cognitive impairment, diagnosis also requires evidence of objective cognitive decline that interferes with daily functioning. Evidence of cognitive decline can be established through family concerns along with standard neuropsychological testing (APA, 2022). Biomarkers—measures of amyloid and tau proteins through spinal fluid, positron emission topography (PET) imaging, and newer blood tests—are being used to support diagnosis by identifying Alzheimer’s-related brain changes (Hansson, 2021).

            14.3.1.1. Causes of Alzheimer’s disease. Autopsies of individuals diagnosed with Alzheimer’s disease identify two abnormal brain structures beta-amyloid plaques and neurofibrillary tangles, both of which are responsible for neuron death, inflammation, and loss of cellular connections (Selkoe & Hardy, 2016). It is believed that beta-amyloid plaques, large bundles of plaque that develop between neurons, appear before the development of dementia symptoms. As these plaque bundles increase in size and number, cognitive symptoms and impaired daily functioning become evident to close family members. Neurofibrillary tangles are believed to appear after the onset of dementia symptoms and are found inside of cells, affecting the protein that helps transport nutrients in healthy cells. Both beta-amyloid plaques and neurofibrillary tangles impact the health of neurons within the hippocampus, amygdala, and the cerebral cortex, areas associated with memory and cognition (Jack et al., 2018).

Researchers have identified additional genetic and environmental influences in the development of Alzheimer’s disorder. Genetically, the apolipoprotein E (ApoE) gene that helps to eliminate beta-amyloid by-products from the brain, has been implicated in the development of Alzheimer’s disorder. One of the three variants of this gene, the e4 allele, appears to reduce the production of ApoE, thus increasing the number of beta-amyloid plaques within the brain. However, not all individuals with the e4 allele develop Alzheimer’s disease; therefore, this explanation may better explain a vulnerability to Alzheimer’s disease as opposed to the cause of the disease.

Various brain regions have also been implicated in the development of Alzheimer’s disease. More specifically, progressive degeneration of neurons within the hippocampus and enthorhinal cortex, areas related to learning and memory, contribute to the early memory impairments of Alzheimer’s disease (Jack et al., 2018; Knopman et al., 2021). As the disease progresses, neurodegeneration spreads to additional regions affecting language, executive functioning, and visuospatial processing. Degeneration acetylcholine-secreting neurons within the basal forebrain reduces availability of acetylcholine, a neurotransmitter essential for attention, learning and memory (Ferreira-Vieira et al., 2016).

Environmental and lifestyle factors may also contribute to the development of Alzheimer’s disease. Recent literature reviews identified cardiovascular disease, hypertension, diabetes, obesity, smoking, physical inactivity, traumatic brain injury, hearing loss, social isolation and lower educational attainment as modifiable risk factors associated with an increased likelihood of dementia (Livingston et al., 2024). Researchers have also investigated environmental exposures, including chronic lead exposure and pollution, as contributors to cognitive decline. While evidence for both lifestyle and environmental factors may increase the risk of dementia, however, they have not been liked as direct causes of Alzheimer’s disease (Livingston et al., 2024; National Institute of Aging, 2024).

            14.3.1.2. Onset of Alzheimer’s disease.  Alzheimer’s disease is often classified according to the age at which symptoms first appear. Early-onset Alzheimer’s disease occurs before the age of 65 and accounts for fewer than 10% of all Alzheimer’s cases (Ayodele et al., 2021). While only a small percentage of individuals experience early onset of the disease, those that do experience early disease progression appear to have a more genetically influenced condition, resulting in a strong family history of the disorder. Furthermore, individuals with these genetic forms of Alzheimer’s disease often experience a more rapid progression of symptoms (Hoogmartens, 2021; Sheppard & Coleman, 2020).

Late-onset Alzheimer’s disease occurs after the age of 65 and represents majority of the cases. Unlike early-onset disease, late-onset Alzheimer’s is influenced by a complex interaction of biological, environmental, and lifestyle factors (Livingston et al., 2024). The APOE ε4 allele is the strongest genetic risk factor for late-onset Alzheimer’s disease. With that said, many individuals with the allele never develop dementia and many patients with Alzheimer’s do not carry the gene. Additional risk factors such as age, cardiovascular health, physical inability, smoking and other lifestyle factors play a central role in the development of Alzheimer’s disease (Belloy et al., 2019).

 

14.3.2. Traumatic Brain Injury (TBI)

TBIs occur when an individual experiences significant trauma or damage to the head, resulting in temporary or permanent disruption of neurological functioning. Neurocognitive disorder due to TBI is diagnosed when persistent cognitive impairment is observed immediately following the head injury, along with one or more of the following symptoms: loss of consciousness, posttraumatic amnesia, disorientation and confusion, or neurological impairment (APA, 2022).

The presentation of symptoms with TBI varies among individuals and depends largely on the location of the injury and the intensity of the trauma. Common symptoms include headaches, disorientation, dizziness, confusion, irritability, fatigue, poor concentration, memory problems, sleep disturbances, and emotional changes. More severe injuries can result in more significant neurological symptoms such as seizures, paralysis, and visual disturbances. While many individuals recover within weeks or months, some experience persistent symptoms known as post-concussive symptoms, which may affect cognitive, emotional, and behavioral functioning (REF).

Major or mild NCD due to TBI occurs frequently alongside other psychological conditions including depressive disorders, anxiety disorders, or personality disorders and PTSD. Individuals with a history of TBI also demonstrate increased rates of suicidal thoughts and behaviors compared to individuals without a TBI history. In fact, rates of suicidal ideation are as high as 10% with rates of suicide attempt hovering around 0.8% to 1.7% (APA, 2022).

The most common type of TBI is a concussion. A concussion occurs when there is a significant blow to the head, followed by temporary changes in brain functioning. Concussions may result in symptoms such as immediate disorientation or loss of consciousness, headaches, dizziness, nausea, and sensitivity to light and noise, and changes in cognition or mood (Patricios et al., 2023). While symptoms of a concussion are usually temporary, there can be more permanent damage due to repeated concussions, particularly if they are close in time.

One area of increased research attention is chronic traumatic encephalopathy (CTE), a progressive, neurodegenerative condition associated with repeated head trauma. CTE is characterized by abnormal accumulation of phosphorylated tau protein in specific brain regions and has been identified most in individuals with repeated head trauma, including athletes (i.e., football players) and military personnel (McKee, 2020). With that said, research on the relationship between repetitive head impacts, CTE pathology, and clinical symptoms is complex, with no clear pathway identified. Difficulty in both diagnosis and research remains challenging because definitive diagnosis requires postmortem neuropathological examination (McKee et al., 2023; McKee, 2020).

 

14.3.3. Vascular Disorders

Neurocognitive disorders due to vascular disorders can occur from a one-time event, such as a stroke, or from ongoing subtle disruptions of blood flow within the brain (APA, 2022). One major contributor to vascular disease is atherosclerosis, a process in which fatty deposits (plaque) and other substances accumulate within blood vessel walls, causing narrowing of the arteries and reduced blood flow. As blood flow to the brain is interrupted, neurons may become damaged or die, resulting in cognitive impairment and stroke (APA, 2022).

Strokes are generally classified into two major categories: an ischemic stroke, when a blot clot or other obstruction blocks the blood flow through the cerebral artery and a hemorrhagic stroke, when a blood vessel ruptures and causes bleeding within the brain (American Stroke Association, 2017). Although strokes can occur at any age, the risk increases substantially with advancing age, particularly after age 65 (Virani et al., 2024). Following a stroke, individuals may experience a wide range of cognitive, behavioral, and emotional changes depending on the location of the stroke and the extent of brain injury. Common deficits after a stroke include difficulties with attention, processing speed, executive functioning, memory, language and emotion regulation (Mok et al., 2024).

Vascular disease is one of the leading causes of neurocognitive impairment and is the second most common cause of dementia after Alzheimer’s disease. Like Alzheimer’s disease, risk factors for vascular cognitive impairment include hypertension, smoking, obesity, high cholesterol and cardiovascular disease. Depression and other psychological disorders are also observed following a stroke, which may complicate recovery and impact treatment outcome (Livingston et al., 2024; Mok et al., 2024).

 

14.3.4. Substance/Medication-Induced Major or Mild NCD

Significant cognitive changes may occur due to repetitive drug and alcohol abuse. Substance intoxication, withdrawal, or the use of multiple substances within a short period can contribute to delirium, which is characterized by disturbances in attention, awareness and cognition (APA, 2022). While delirium symptoms are often transient during these states, resolving when intoxication or withdrawal subsides, persistent cognitive changes may present due to prolonged substance misuse. Symptoms or mild or major neurocognitive disorder due to substance use can range from impairments in attention, executive functioning, learning, memory, and processing speed depending on the substance and duration of use (Lunga et al., 2025; APA, 2022).

 

14.3.5. Dementia with Lewy Bodies

Symptoms associated with neurocognitive disorder due to Lewy bodies include significant fluctuations in attention and alertness, recurrent visual hallucinations, sleep disturbances, and spontaneous features of Parkinson’s such as tremor, slowed movement, and impaired balance (APA, 2022). Cognitive changes often involve attention, executive functioning and memory impairment. While the trajectory of the illness varies for each individual due to overall general health at the time of illness onset, research suggests that most individuals do not survive longer than seven years post-diagnosis (Lewy Body Dementia Association, 2026).

Lewy bodies are irregular brain cells that result from the buildup of abnormal proteins (alpha-synuclein) in the nuclei of neurons. The widespread distribution of Lewy bodies damages neurons and causes dysfunction in several neurotransmitter systems including acetylcholine and dopamine. The reduced acetylcholine activity is associated with cognitive and attentional difficulties, whereas the degeneration of dopamine neurons contributes to the movement related symptoms (National Institute on Aging, 2024).

 

14.3.6. Major or Mild Frontotemporal NCD

Frontotemporal NCD causes “progressive development of behavioral and personality change and/or language impairment” (APA, 2022, pg. 696). For the behavioral variant, individuals display at least three of the following: behavioral disinhibition, apathy or inertia, loss of sympathy or empathy, preservative or compulsive behavior, or hyperorality and dietary changes. For the language variant, they show prominent decline in language ability (i.e., speech production, word finding, object naming, grammar, or word comprehension). There is relative sparing of learning and memory and perceptual-motor functioning. Individuals with frontotemporal NCD commonly present in their 50s though the age of onset has a range of age 20 to 80 years. The median survival is 6-11 years after symptom onset and 3-4 years after diagnosis (APA, 2022).

 

14.3.7. Parkinson’s Disease

The awareness of Parkinson’s disease has increased in recent years, in part due to public figures such as Michael J. Fox sharing their experience with the disorder. Parkinson’s disease is a progressive neurodegenerative disorder that affects approximately 500,000 to one million individuals in the United States (National Institute of Neurological Disorders [NINDS], 2025). The disorder occurs when dopamine-producing neurons, particularly those in the substantia nigra, become damaged and die, resulting in disruptions in movement and other brain functions (NINDS, n.d.).

The four main symptoms of Parkinson’s disease include resting tremor, rigidity of the limbs and trunk, bradykinesia (slowness in initiating and performing movements), and impaired balance and coordination (National Institute on Again [NIA], 2022). While these motor symptoms are among the most noticeable, many individuals with Parkinson’s disease also experience depression, anxiety, sleep disturbances, apathy and cognitive changes. (NIA, 2022).  These motor symptoms are generally present at least one year prior to the beginning of cognitive decline, although severity and progression of symptoms vary significantly from person to person.

Onset of Parkinson’s disease ranges from age 50 to 89 years. Mild NCD develops early in the course of Parkinson’s disease while Major NCD does not occur until individuals are much older. The prevalence of Parkinson’s disease in the U.S. increases with age and is more common in men than women. The disease is comorbid with Alzheimer’s disease and cerebrovascular disease. Depression, psychosis, REM sleep behavior disorder, apathy, and motor symptoms can make functional impairment worse (APA, 2022).

 

14.3.8. Huntington’s Disease

Huntington’s disease is a rare genetic disorder that is characterized by progressive motor dysfunction, cognitive decline, and psychiatric symptoms. Due to the progressive and degenerative nature of the disorder, symptoms typically worsen over time and therefore, is associated with a shortened life-expectancy, with most individuals surviving only 15-20 years post-onset of symptoms (NINDS, 2025). Although symptoms can present at any time, the average age of symptom presentation is during middle adulthood (between ages 35 and 45 years; APA, 2022). Symptoms generally begin with neurocognitive decline, particularly in executive function, along with changes in mood and personality. As symptoms progress, more physical symptoms present, such as facial grimaces, difficulty speaking, and repetitive movements. Because there is no treatment for Huntington’s disease, the severity of the cognitive and physical impairments ultimately leads to complete dependency and the need for full-time care. Suicide is among the leading causes of death in Huntington’s disease (APA, 2022).

 

14.3.9. HIV Infection

Not many people are aware that cognitive impairment is sometimes the first symptom of untreated HIV. While symptoms vary among individuals, slower mental processing, impaired executive function, problems with more demanding attentional tasks, and difficulty learning new information are among the most common early signs (APA, 2022). When HIV becomes active in the brain, significant alterations of mental processes occur, thus leading to a diagnosis of neurocognitive disorder due to HIV infection. Significant impairment can also occur due to HIV-infection related inflammation throughout the central nervous system.

The widespread use of combination antiretroviral therapy (cART) has dramatically reduced the incidence of severe HIV-associated dementia and improved overall life expectancy for individuals living with HIV. With that said, mild forms of HIV-associated neurocognitive impairment continue to affect approximately 20-50% of people living with HIV (Wang et al., 2020). Current research suggests that chronic inflammation, cardiovascular risk factors and other medical conditions likely contribute to the ongoing cognitive difficulties, even among individuals receiving effective treatment. Therefore, future research is focused on identifying strategies to prevent and treat neurocognitive complications while improving long-term health.

 

 

---

14.4. Treatment

 

Section Learning Objectives

• Describe treatment options for neurocognitive disorders.

 

Treatment options for neurocognitive disorders remain limited, particularly for disorders involving progressive neurodegeneration. Current interventions typically focus on reducing symptoms, maintaining functioning, and improving quality of life. Because many neurodegenerative disorders involve ongoing changes in the brain, treatments often aim to slow decline rather than restore lost cognitive abilities.

 

14.4.1. Pharmacological

Pharmacological interventions have been most extensively studied in Alzheimer’s disease. Medications designed to target acetylcholine and glutamate, have been the most effective treatment options in alleviating symptoms and reducing the speed of cognitive decline within individuals diagnosed with Alzheimer’s disease. Specific medications such as donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne) increase acetylcholine availability and may temporarily improve or stabilize cognitive symptoms. Memantine (Namenda), an NMDA receptor antagonist, regulates glutamate activity and is commonly used in moderate to severe Alzheimer’s disease (APA, 2022; Alzheimer’s Association, 2025).

Most recent advancements have resulted in the approval of treatments targeting beta-amyloid accumulation. Lecanemab (Leqembi) and donanemab (Kisunla) are monoclonal antibodies that reduce amyloid plaques and have demonstrated slowing of cognitive and functional decline in individuals with early Alzheimer’s disease. These medications require careful monitoring due to significant and adverse reactions (Alzheimer’s Association, 2026a).

Parkinson’s disease has also found success in pharmacological treatment options. The medication Levodopa increases dopamine availability, which provides relief of both physical and cognitive symptoms. Unfortunately, there are also significant side effects such as dyskinesias, hallucinations, and psychotic symptoms. Additional medications and nonpharmacological interventions are often combined to address motor, cognitive, and emotional symptoms associated with Parkinson’s disease (APA, 2022).

 

14.4.2. Psychological

Among the most effective psychological treatment options for individuals with neurocognitive disorders are the use of cognitive and behavioral strategies designed to maintain functioning and improve quality of life. Cognitive stimulation activities including computer-based cognitive stimulation programs, problem-solving tasks, reading books, and following the news, have been associated with improvements in cognitive functioning and quality of life among individuals with dementia (Livingston et al., 2024).

Behavioral interventions focused on supporting independence by engaging in social skills and self-care training, as well as modifying the environment, have been shown to improve functioning in individuals with neurocognitive deficits. For example, by breaking down complex tasks into smaller, more attainable goals, as well as simplifying the environment (i.e., labeling location of items, removing clutter), individuals can successfully engage in more independent living activities.

 

14.4.3. Support for Caregivers

Supporting caregivers is an important component of treatment because caring for an individual with a neurocognitive disorder often places substantial emotional, physical, and financial demands on caregivers.  Most individuals living with neurocognitive disorders receive care from family members or other unpaid caregivers (Alzheimer’s Association, 2026b). The chronic stress of caregiving has been associated with increased rates of depression, anxiety, caregiver burden, sleep disturbance and overall poorer physical health (Livingston et al., 2024). Given this, it is important that healthcare providers routinely assess caregivers’ psychological well-being and encourage participation in caregiver support groups, psychoeducation programs, respite services, and individual psychotherapy as needed.

 

1. Review the listed treatment options for neurocognitive disorders. What are the main goals of these treatments?

 

---

Module Recap

Our discussion in Module 14 turned to neurocognitive disorders to include the categories of delirium, major neurocognitive disorder, and Mild neurocognitive disorder. We also discussed the subtypes of Alzheimer’s disease, traumatic brain injury (TBI), vascular disorder, substance/medication induced, dementia with Lewy bodies, frontotemporal NCD, Parkinson’s disease, Huntington’s disease, and HIV infection. The clinical description, epidemiology, etiology, and treatment options for neurocognitive disorders were discussed.

---

 

End Module 14

4th edition as of August 2026