Treatments for Neurocognitive Disorders

Learning Objectives

  • Describe psychological perspectives and treatments for neurocognitive disorders

In this course, we have learned to assess and analyze disorders from multiple psychological perspectives, such as the psychodynamic, biological, humanistic, behavioral, and cognitive perspectives. Neurocognitive disorders, by definition, mostly relate to the cognitive perspective, as the cognitive perspective views psychological disorders as originating from an interruption, whether short or long, in our basic cognitive functions, i.e., memory processing, perception, problem-solving, and language. All the neurocognitive disorders have biological causes, as explained in the previous readings, because they are attributed to biological changes caused by Alzheimer’s, Parkinson’s, Huntington’s disease, HIV, traumatic brain injury (TBI), or other illnesses. The focus in understanding and treating neurocognitive disorders lies then in understanding the biological changes and what measures can be taken to slow cognitive decline. There is evidence that some measures are effective in preventing or slowing the progression of cognitive symptoms.

Recall that major neurocognitive disorder (MND) is a syndrome that progresses with significant deterioration of cognitive domains as compared to previous levels of cognitive performance in memory, speech, reasoning, intellectual function, and/or spatiotemporal perception, and may also be associated with changes in emotional behavior and difficulties at the functional level. The decline is initially noticed by the individual, the family, or the general practitioner (GP) who is usually responsible for the early diagnosis (American Psychiatric Association [APA], 2014).

MND may result from brain disorders, classified as primary (degenerative), or be a consequence of other conditions (secondary) (Emre, 2009). The most common types of MND are Alzheimer’s disease, vascular dementia (VaD), Lewy body dementia, and frontotemporal dementia (FD). In secondary MND (e.g., alcoholic dementia and infectious diseases), the symptoms may be treated and/or prevented. Therefore, a correct diagnosis is crucial for proper disease management and treatment. This is supported by a detailed collection of the person’s clinical history, neurological and neuropsychological examination, and the comprehensive use of laboratory and imaging tests. In primary MND, early diagnosis is equally crucial either to delay the progression of cognitive symptoms and to control/stabilize psychiatric manifestations (Ribeira et al., 2004).

Predictive Factors of MND

MND is likely to develop in a continuous process (Brooks and Loewenstein, 2010). Individual factors affect the likelihood of developing MND and these factors predicting the development of the disease should be known. If known, preventive interventions may prevent or protect people at risk of MND.

Previous studies have identified predictive factors of MND, which can be grouped into the following:

  • sociodemographic factors (e.g., sex, age, and years spent in education and social isolation)
  • health factors (e.g., hearing loss, cardiovascular diseases, hypertension, diabetes, handgrip strength, and nutritional status)
  • bio-behavioral factors (e.g., smoke, alcohol, and physical activity) (Helzner et al., 2009; Nagai et al., 2010; Polidori et al., 2012; Baumgart et al., 2015; Santana et al., 2015; Schwarzinger et al., 2018)

Given that most of these factors are all potentially modifiable (e.g., diabetes, cholesterol, depression, or malnutrition; Chen et al., 2017), the individual can play an active role in the prevention or management of MND, which creates the opportunity to allow for more efficient intervention. Primary prevention in the primary health care context is important for the course of MND and should focus on the identification of situations that increase the likelihood of occurrence or worsening of symptoms. However, few studies identify predictive factors associated with the severe stage of MND (Eshkoor et al., 2016).

A study by Sousa, Laetitia Teixeira, and Constança Paúl identified four predictors of MND including age, years spent in education, physical activity, and hand strength. Physical activity, hand strength, and education play a protective role (“the more the better”). On the other hand and as expected, while age increases, the risk of MND also increases.[1]

There is extensive and persuasive evidence from mechanistic and well-designed prospective cohort studies that reducing the exposure to high blood pressure and hypertension in mid-life and to diabetes in mid-and late life, reducing tobacco use, and increasing the education level of populations can effectively reduce the dementia risk for populations (Prince et al, 2014).

Treating Neurocognitive Disorders

There is no cure for neurocognitive disorders or the diseases that cause them. Pharmacological approaches combined with behavioral and environmental interventions are most successful in treating neurocognitive disorders.

A person getting their blood pressure checked by a nurse.

Figure 1. High blood pressure is a vascular risk factor for developing a neurocognitive disorder.

Antidepressants, antipsychotics, and other medications that treat memory loss and behavioral symptoms are also available and may help to treat the diseases. Ongoing psychotherapy and psychosocial support for patients and families are usually necessary for clear understanding and proper management of the disorder and to help maintain a better quality of life for caregivers and patients. In addition, speech therapy has been shown to help neurocognitive dementia patients with language impairment.

Studies suggest that diets with high Omega 3 content and low in saturated fats and sugars, along with regular exercise can increase the level of brain plasticity. Other studies have shown that mental exercise such as newly developed computerized brain training programs can also help build and maintain targeted specific areas of the brain. These studies have been very successful for those diagnosed with schizophrenia and can improve fluid intelligence and the ability to adapt and deal with new problems or challenges the first time encountered; in young people, it can still be effective in later life.

A person with amnesia may slowly be able to recall their memories or work with an occupational therapist to learn new information to replace what was lost or to use intact memories as a basis for taking in new information. If amnesia is caused by an underlying cause such as Alzheimer’s disease or infections, the cause may be treated but the amnesia may not be.

Pharmacological Interventions

Targets for pharmacological treatment include

  • cognitive impairment (e.g., memory loss, disorientation, and decrease in attention and problem-solving).
  • behavioral symptoms (e.g., agitation and aggression).
  • psychological symptoms (e.g., depression, anxiety, and psychosis).

There is a large body of evidence for the efficacy of cholinesterase inhibitors (ChEIs), such as donepezil, rivastigmine, and galantamine, in the treatment of mild to moderate Alzheimer’s disease (Institute for Quality and Efficiency in Healthcare, 2014). The use of each of these medications is associated with modest and short-term comparable improvements in cognitive function, global clinical state, and activities of daily living. However, the evidence base for cholinesterase inhibitors (ChEIs) in low- and middle-income countries is limited. Moreover, the efficacy of this class of drugs in severe dementia is unclear, although behavioral symptom improvement was identified for galantamine (Institute for Quality and Efficiency in Healthcare, 2014). A fourth drug for the treatment of cognitive impairment, memantine, has a different mode of action and is well tolerated, but evidence for its efficacy is limited to people with moderate to severe dementia. Cholinesterase inhibitors (ChEIs) and memantine are less efficacious in vascular dementia than other forms. ChEIs and memantine’s efficacy in the treatment of behavioral disturbances is not established; manufacturer-sponsored licensing trials and post hoc analyses indicate small improvements.

A small bottle of Haloperidol.

Figure 2. Haloperidol is an atypical antipsychotic medication that can be administered through injection.

Use of haloperidol and atypical antipsychotic medications for the treatment of agitation and behavioral  and psychological symptoms of dementia (BPSD) indicate small treatment effects, most evident for aggression, although these must be weighed against the associated mortality risk (Kales et al, 2012). Atypical antipsychotic drugs have been widely prescribed for psychosis in dementia, but a meta-analysis of their efficacy indicated that only aripiprazole and risperidone had a statistically and clinically significant effect on psychiatric symptoms (Tan et al, 2015). An important caveat to the use of these medications in dementia is the associated increased risk of death and cerebrovascular adverse events. The literature on antipsychotic treatment in older people with dementia reveals that although improvement in the behavioral disturbance was minimal after six to 12 weeks, there was a significant increase in absolute mortality risk of approximately 1% (Banerjee et al, 2009). The literature suggests that prescribing antipsychotics in dementia beyond six to 12 weeks is likely to be substantially harmful in continued antipsychotic treatment in dementia. Therefore, many recommend nonpharmacological treatments, such as psychological and training interventions, to reduce BPSD rather than antipsychotic management (Duedon et al, 2009). A meta-analysis of the efficacy of antidepressants in people with dementia was inconclusive (Leong, 2014). Antidepressants have been proposed for the treatment of BPSD with encouraging results (Henry et al, 2011).

Nonpharmacological Interventions

A well-conducted randomized control trial of cognitive stimulation (reality orientation, games, and discussions based on information processing rather than knowledge) conducted in the United Kingdom as a group intervention, and a small pilot trial from Brazil, suggest that cognitive benefits from this intervention are similar to those for ChEIs (Aguirre et al, 2013). More specific cognitive training produced no benefits. Cognitive rehabilitation, an individualized therapy designed to enhance residual cognitive skills and the ability to cope with deficits, showed promise in uncontrolled case series in hospital incident command systems. A meta-analysis of four trials of reminiscence therapy (the discussion of past activities, events, and experiences) provides evidence for short-term improvement in cognition, mood, and caregiver strain, but the quality of these trials was poor (Bahar-Fuchs, 2013; Woods et al, 2005; Woods et al, 2012).

In terms of nonpharmacologic therapies, cognitive stimulation therapy has been shown to be cost-effective for people with mild-to-moderate dementia when delivered biweekly over seven weeks, though was found to have modest effects when continued for longer when added to administration of acetylcholinesterase inhibitors (D’Amico et al, 2015). An exercise intervention was found to have the potential to be cost effective when considering behavioral and psychological symptoms, but did not appear cost effective when considering quality-adjusted life year gains. The START (Strategies for Relatives) study, a randomized controlled trial to determine the clinical effectiveness and cost-effectiveness of a manual-based coping strategy program in promoting the mental health of carers of people with dementia, found the intervention to be cost effective with respect to the caregiver and patient outcomes, and National Institute for Health and Care Excellence (NICE) thresholds (Livingston et al, 2014). In a health economic analysis of resource costs and costs of formal care on a psychosocial intervention for family caregivers of persons with dementia, those in the intervention group reported a higher quality of life while their spouse was living at home (Dahlrup et al, 2014).

Deep brain stimulation (DBS) is a neurosurgical procedure involving the placement of a medical device called a neurostimulator (sometimes referred to as a brain pacemaker), which sends electrical impulses, through implanted electrodes, to specific targets in the brain (brain nuclei) for the treatment of movement and some neurocognitive disorders, including Parkinson’s disease and epilepsy. Deep brain stimulation (DBS) is used to manage some of the symptoms of Parkinson’s disease that cannot be adequately controlled with medications. Deep brain stimulation (DBS) is recommended for people who have Parkinson’s disease with motor fluctuations and tremor inadequately controlled by medication, or to those who are intolerant to medication, as long as they do not have severe neuropsychiatric problems. Four areas of the brain have been treated with neural stimulators in Parkinson’s disease. These are the globus pallidus internus, thalamus, subthalamic nucleus and the pedunculopontine nucleus. However, most DBS surgeries in routine practice target either the globus pallidus internus, or the subthalamic nucleus. Generally DBS is associated with 30–60% improvement in motor score evaluations.[2]

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Glossary

deep brain stimulation: a neurosurgical procedure involving the placement of a medical device called a neurostimulator that sends electrical impulses, through implanted electrodes, to specific targets in the brain

  1. Sousa, Susana, Laetitia Teixeira, and Constança Paúl. “Assessment of Major Neurocognitive Disorders in Primary Health Care: Predictors of Individual Risk Factors.” Frontiers in Psychology 11 (2020): 1413. https://doi.org/10.3389/fpsyg.2020.01413. ↵
  2. Thakur KT, Albanese E, Giannakopoulos P, et al. Neurological Disorders. In: Patel V, Chisholm D, Dua T, et al., editors. Mental, Neurological, and Substance Use Disorders: Disease Control Priorities, Third Edition (Volume 4). Washington (DC): The International Bank for Reconstruction and Development / The World Bank; 2016 Mar 14. Chapter 5. Available from: https://www.ncbi.nlm.nih.gov/books/NBK361950/ doi: 10.1596/978-1-4648-0426-7_ch5 ↵