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With many women in perimenopause experiencing a subjective sense of change in cognitive function, understanding normal cognitive function in perimenopause is important for clinicians in day-to-day practice. This chapter aims to equip mental health professionals with the knowledge and confidence to appropriately explore cognitive concerns arising during the perimenopause. The chapter outlines normal cognitive function in perimenopause, exploring symptoms and how they may present, as well as aiming to identify who may be at greater risk from cognitive change. It then offers suggestions on how to support women to reduce symptoms of cognitive dysfunction as far as is practicable. The chapter later explores the role of hormone replacement therapy (HRT) on both cognition in perimenopause and beyond into postmenopause, as well as considering the impact HRT has on the brain and risk of dementia in later life. With up to 45% of dementia now felt to be preventable, the chapter discusses the role of the healthcare professional in identifying risks presenting around the time of perimenopause, allowing clinicians to then offer intervention and promote good brain health in mid-life leading into later-life.
Edited by
Katherine Warburton, California Department of State Hospitals, University of California, Davis, USA,Stephen M. Stahl, University of California, Riverside, USA
Schizophrenia is a highly heterogenous disorder with substantial interindividual variationin how the illness is experienced and how it presents clinically. The disorder is composed of primary symptom clusters—positive symptoms, negative symptoms, disorganization, neurocognitive deficits, and social cognitive impairments. These, along with duration, severity, and excluding other possible etiologies, comprise the diagnostic criteria for the disorder outlined in the two commonly used diagnostic classification systems—the Diagnostic Statistical Manual of Mental Disorders, Fifth Edition, Text Revision and the International Classification of Diseases, 11th Revision. These primary symptoms as well as accessory symptoms (mood disturbances, anxiety, violence) and comorbidities (substance use, suicidality) bear upon each other to varying degrees and impact functionaloutcomes. The following review presents two patient cases illustrating the clinical heterogeneity of schizophrenia, the natural history of the illness and diagnosis, followed by the current understanding of the primary symptom clusters, accessory symptoms, and comorbidities. In addition to noting symptom prevalence, onset, and change over time, attention is paid to the impact of symptoms on functional outcome.
Lifestyle changes and unhealthy eating habits have led to a sharp rise in obesity rates worldwide. Obesity is closely associated with a range of complications, including cognitive impairment and dementia. Accumulating evidence indicates that obesity negatively affects cognitive function and may increase the risk of neurodegenerative diseases. Conversely, cognitive dysfunction may further contribute to the development and progression of obesity. With growing attention in this field, obesity-related cognitive impairment has emerged as an important research focus at the intersection of metabolic and neurological disorders.
Methods
This article reviews the potential mechanisms underlying obesity-related cognitive impairment and summarizes emerging therapeutic strategies.
Results
The development and progression of obesity-related cognitive impairment involve multiple mechanisms, including insulin resistance, systemic and central inflammation, immune dysregulation, microcirculatory alterations and changes in neurotransmitters and synaptic plasticity. Recent studies have focused on the adipose tissue-brain axis and the microbiota–gut–brain axis, in particular, the targeted effects of extracellular vesicles released from adipose tissue and microbiota on the brain.
Conclusions
This article systematically reviews the mechanisms underlying obesity-related cognitive impairment and presents novel therapeutic strategies.
Substance use disorder (SUD) is frequently associated with cognitive impairment that negatively affects treatment adherence and clinical outcomes. Neuropsychological assessments provide detailed information but are often impractical in clinical settings, underscoring the value of brief but sensitive tools such as the Montreal Cognitive Assessment (MoCA).
Aims
This study aimed to evaluate the utility of MoCA in detecting cognitive impairment in SUD, examining cognitive recovery following sustained abstinence, exploring gender differences in cognitive progression and determining whether baseline cognitive performance predicts treatment dropout.
Method
Ninety-five SUD patients and 57 healthy controls completed MoCA at baseline and were reassessed after 6 months.
Results
At baseline, 72.60% of individuals demonstrated cognitive impairment compared with controls, with deficits evident in both global cognition and visuospatial/executive, attention, memory and language domains. Following 6 months of abstinence, deterioration rates decreased to 50%, indicating substantial but not complete recovery, because the improvement in overall cognition was moderate. Male patients showed significantly greater cognitive gains than female patients, particularly in visuospatial/executive and digit span performance. Patients impaired at baseline reported more severe alcohol use and earlier onset of cannabis use disorder. Patients with cocaine use disorder showed the poorest recovery and the highest rate of treatment dropout. Lower baseline language and fluency scores were strongly associated with treatment discontinuation. Language deficits, together with cocaine use disorder, predicted 69% of dropout cases.
Conclusions
Findings indicate MoCA as a practical screening tool for early detection of cognitive impairment, longitudinal monitoring and personalised treatment planning in SUD.
What is the next step in treating a primary psychotic illness with aggression when high-dose/high-level clozapine treatment only provides a partial response?
Extensive evidence links air pollution exposure to cognitive decline; however, it remains unclear whether cognitive reserve and brain reserve modify this association. We examined the moderating roles of cognitive reserve contributors and brain reserve in the association between air pollution and cognitive function in dementia-free adults.
Methods
Cross-sectional data were obtained from 650 participants who underwent 3T brain magnetic resonance imaging and completed the Montreal Cognitive Assessment (MoCA). Cognitive reserve contributors were assessed based on education, occupation, and social engagement. Brain reserve was quantified using the ventricle-to-brain ratio derived from brain scans. Five-year average concentrations of particulate matter with diameters ≤10 and ≤2.5 μm and nitrogen dioxide were estimated based on residential addresses. Partial least squares structural equation modeling was applied to construct latent variables representing the air pollution mixture and composite cognitive reserve (contributors). Analyses examined whether cognitive reserve contributors and brain reserve modified associations of air pollution with MoCA scores and suspected mild cognitive impairment.
Results
In individuals with an average level of cognitive reserve, a 1–standard deviation increase in air pollution mixture was associated with a 0.24-point decrease in MoCA scores (95% confidence interval [CI]: −0.31 to −0.16). This association was attenuated in individuals with higher cognitive reserve (β = −0.12; 95% CI: −0.25 to 0.02) and intensified in those with lower cognitive reserve (β = −0.36; 95% CI: −0.37 to −0.35). The moderating effect of brain reserve was not significant.
Conclusions
Higher cognitive reserve may mitigate the effects of air pollution on cognitive function.
Cognitive impairment in the ICU can have long-term, life-altering impacts well beyond the ICU and hospital stay. Cognitive impairment can be hard to identify in the complex medical setting of the ICU, but the systematic use of standardized screens and assessments can alert the write as healthcare team to cognitive impairment. Patients with disorders of consciousness benefit from cognitive stimulation interventions. For patients awake and alert, cognitive intervention strategies include cognitive training (e.g., word search, memory match) and cognitive rehabilitation (e.g., ADL and IADL performance). Early engagement in activity in the ICU can help improve overall performance. One component of rehabilitation is functional cognition, defined as the process of utilizing and integrating thinking and processing skills to accomplish everyday activities. Assistive technology is another tool that can help patients with tasks from communication to complex problem solving and executive functioning. Cognitive stimulation, training, and rehabilitation all work toward decreasing the impact of cognitive impairments and improving overall function and quality of life. Examining patients’ performance through real-life functional tasks help to generalize these skills.
Survivors of critical illness are at increased risk for the development of functional impairments, including difficulties performing activities of daily living and instrumental activities of daily living. This chapter explores the role of occupational therapy (OT) in the rehabilitation of patients impacted by post intensive care syndrome (PICS). Specific evaluation tools used by occupational therapists that can be assess PICS patients to identify their impairments in the key areas of physical, cognitive, and mental health are described. Thereafter, interventions used by occupational therapists to remediate identified impairments and maximize independence are described, derived from a combination of evidence-informed practice in similar patient populations and current empirical evidence for PICS rehabilitation.
Delirium, which is an important risk factor for post-intensive care syndrome (PICS), is common during critical illness, affecting between 20% and 80% of patients. It is associated with numerous adverse outcomes, including longer time on mechanical ventilation, longer time in the intensive care unit (ICU) and hospital, death, and long-term cognitive impairment. Delirium in the ICU can be reliably detected using multiple tools, including the Confusion Assessment Method in the ICU (CAM-ICU) and the Intensive Care Delirium Screening Checklist (ICDSC). The exact cause of delirium, however, remains elusive even though there are many purported mechanisms, including neuroinflammation, metabolic insufficiency, neuronal dysfunction, and neurotransmitter disturbances. Due to knowledge gaps regarding the mechanism(s) of delirium, effective medical treatments for delirium also remains elusive. Current practice involves the prevention of delirium through the recognition and management of modifiable risk factors. The well-studied ABCDEF bundle is one such strategy, which is primarily non-pharmacologic, to prevent or mitigate delirium and thus limit its adverse outcomes. Unfortunately, delirium still occurs at a high rate, and the work to understand the underlying mechanism and its varied manifestations and to develop an effective treatment continues.
More than five million individuals in North America experience an episode of critical illness annually, and among those who survive, as many as a third experience substantial cognitive impairment, which often lasts long after discharge and can be permanent. While cognitive impairment after critical illness has been widely studied for two decades, much remains unknown, and the insights that have been generated by research often fail to inform clinical care. Key issues germane to understanding and optimally treating ICU survivors with cognitive deficits include: improving methods of early detection and screening, honing and implementing cognitive rehabilitation strategies, and better understanding the trajectories of impairments observed in patients. Prioritizing the brain health of individuals after critical care both through prevention and thoughtful interventional efforts remains a key public health goal and one that can only be accomplished through careful and deliberate interdisciplinary efforts.
It is estimated that, worldwide, a new case of dementia develops every 3 s. Around 60% of cases occur in low- and middle-income countries such as Egypt, with this number expected to rise to 71% in the next 25 years. Egypt is the most populous Arabic-speaking country, containing one-quarter of the world’s Arab population. However, a majority of tools for assessing cognitive impairment have not been standardised, normed and validated according to International Test Commission guidelines, nor have they been culturally adapted, for the Egyptian population. We gathered insight from doctors and clinicians practising in Egypt to learn how they assess patients suspected of cognitive impairment. The majority reported that they used Western-made screening tools (e.g. the Montreal Cognitive Assessment), but were overwhelmingly of the view that such assessments should be standardised and adapted for Egyptians. This lack of consistent standards can lead to misclassification of cases in this lower middle-income country.
Music is associated with reduced pain, anxiety, and sedative requirements in ICU patients. Slow-tempo music (60 to 80 beats per minute) in particular has been associated with a neuromodulatory effect. The minimum duration of music listening associated with decreased pain may be as brief as 20 to 30 minutes, resulting in a nearly 2-point decrease in self-reported pain scores (on a 0-10 scale). Longer duration of music listening (i.e., more than 45 minutes) is associated with improved sleep quality and less depressive symptoms after critical illness. Through its interaction with various cortical areas, music may also offer beneficial effects on cognition. Neurocognitive processing of music invokes brain centers related to emotion, perception, cognition, and the autonomic nervous system. In EEG and functional MRI studies, music increased communication between the functional neural networks typically disrupted in delirium and dementia. Whether music listening in ICU patients with delirium can improve long-term cognitive function is not clearly understood but is being evaluated in randomized controlled trials. Ongoing clinical and scientific work will lay the groundwork to identify the neuroprotective mechanisms by which music may reduce the risk of ICU delirium and long-term cognitive impairments.
Lewy body disease (LBD) can present as a dementia-predominant syndrome with parkinsonism (dementia with Lewy bodies or DLB), a motor-predominant syndrome with subsequent dementia ( Parkinson’s disease with dementia or PDD), or an autonomic-predominant syndrome (multiple system atrophy or MSA); this chapter focuses on treatment/management of the many complex manifestations of DLB. Education and support are important in managing DLB. Currently, there is no therapy that significantly alters the underlying pathophysiology of DLB. This chapter covers the management of cognitive impairment, neuropsychiatric features, motor dysfunction, sleep disorders, and autonomic dysfunction. Acetylcholinesterase inhibitors (AChEI) can improve cognition. Memantine may provide modest benefit. Medications such as clozapine or quetiapine can help manage visual hallucinations and delusions. Carbidopa/levodopa and dopamine agonists can improve motor symptoms, but caution is needed. Clonazepam, melatonin, and psychostimulants can address sleep issues. Orthostatic hypotension can be managed with lifestyle changes and medications.
Normal pressure hydrocephalus (NPH) is divided into idiopathic (iNPH) and secondary causes such as tumors, infections, trauma, or intracranial hemorrhage. More people are now overweight, and BMI correlates with CSF pressure so many patients have higher CSF pressure making the “normal” in NPH a partial misnomer. The dominant symptom is gait impairment often accompanied by cognitive and urinary difficulty. NPH requiring treatment is relatively rare but potentially underdiagnosed. A clinical approach to NPH should start with a differential diagnosis of the gait difficulty, as in early stages, patients may not have the full symptom triad. Those with anomia may have Alzheimer’s dementia or primary progressive aphasia, and there can be additional patients with concomitant NPH and other disorders such as Alzheimer’s, Parkinson’s, and cervical myelopathy that may require treatment of both pathologies. The most useful diagnostic tests in the workup of NPH include magnetic resonance imaging (MRI) of the brain and a CSF drainage trial, with either high volume lumbar puncture or lumbar drain trial, with the videotaping of the gait before and after the CSF removal. The primary treatment remains a CSF diversion procedure with placement of a shunt, and several shunt surgical advances have resulted in less mortality and morbidity.
This chapter discusses the diagnostic evaluation, physical examination, initial diagnostic formulation, investigations, and management of individuals with cognitive and/or behavioral changes. It emphasizes the importance of obtaining a comprehensive history from the patient and an informant, as well as conducting a thorough physical examination. The chapter also provides sample questions for assessing different cognitive domains and lists clues that suggest a non-Alzheimer’s disease etiology of cognitive/behavioral changes. It suggests various diagnostic studies and consultations that may be necessary for each patient. The document highlights the principles of management, including treating reversible causes, minimizing psychoactive medications, promoting regular sleep and exercise, and providing caregiver support. It also discusses the availability of pharmacologic therapies and the importance of providing information and support to families facing dementia-related issues.
This concurrent, exploratory, mixed-methods process evaluation, embedded within a randomised controlled trial, investigates how the ‘active prevention in people at risk of dementia through lifestyle behaviour change and technology to build resilience’ (APPLE-Tree) secondary dementia prevention intervention might support behavioural and lifestyle goal attainment, through determining the contexts influencing engagement and testing intervention theoretical assumptions.
Aims
We aimed to investigate (a) intervention reach, dose and fidelity, (b) contexts influencing engagement and (c) alignment of findings with theoretical assumptions about how the intervention might have supported participants to meet personalised behavioural and lifestyle goals.
Method
We measured intervention reach and dose. We selected interviewees for setting, gender and ethnic diversity from the 374 APPLE-Tree trial participants randomised to the intervention arm. We interviewed 25 intervention participants, 12 facilitators and 3 study partners. Additionally, we analysed 11 interviews previously conducted during or after intervention delivery for an ethnography, and 233 facilitator-completed participant goal records. We thematically analysed data, combining inductive/deductive approaches informed by the ‘capability, opportunity and motivation-behaviour’ (COM-B) behaviour change model. We video-recorded a randomly selected tenth of sessions and rated fidelity.
Results
A total of 346 of 374 (92.5%) intervention arm participants received some intervention (reach), and 305 of 374 (81.6%) attended ≥5 main sessions (predefined as adhering: dose). According to facilitator records, participants met a mean of 5.1 of 7.5 (68.3%) goals set. We generated three themes around (a) building capability and motivation, (b) connecting with other participants and facilitators and (c) flexibility and a tailored approach.
Conclusions
The intervention supported behaviour change, through increasing knowledge and providing space to plan, implement and evaluate new strategies and make social connections. Feedback indicated that the intervention was flexible and inclusive of diverse preferences and needs.
Cognitive impairment is a significant, yet often overlooked, non-motor symptom of Parkinson’s disease, and a strong predictor of quality of life for those affected. Despite the availability of both pharmacological and non-pharmacological treatment options for Parkinson’s disease, their efficacy for the cognitive symptoms of the disease specifically is unclear, as no ‘gold standard’ treatment strategy for cognitive impairment in the disease has yet emerged. Further, a comparative understanding of the efficacy of each of these treatment options is severely lacking.
Aims
This systematic review aims to critically evaluate the efficacy of non-pharmacological interventions for the treatment of cognitive impairment in Parkinson’s disease.
Method
A comprehensive systematic search will be conducted to identify studies involving participants clinically diagnosed with Parkinson’s disease that assess non-pharmacological interventions targeting cognitive impairment. If feasible, results will be synthesised using meta-analysis; otherwise, narrative synthesis will be used.
Results
This is a protocol for a systematic review that is yet to be conducted.
Conclusions
The findings from this review will provide critical insight into the efficacy of non-pharmacological treatment options for cognitive impairment in Parkinson’s disease, which may help to influence clinical recommendations for the treatment of cognitive impairment in Parkinson’s disease and highlight existing gaps in the literature.
White matter hyperintensities (WMH) on fluid-attenuated inversion recovery MRI sequence are regions where fluid from supplying vessels leaks into brain tissue. Some studies have demonstrated an association between WMH and cognitive decline. Given the common WMH risk factors in our local population, the aim of this study is to examine the relationship of overall and regional WMH with cognition in Hamilton, Canada.
Methods:
Adults presenting to Hamilton General Hospital in 2020 with a head MRI and cognitive assessment within 6 months of the MRI were included in our cross-sectional study. MRIs were reviewed, assigning a periventricular (PV), a subcortical (SC) and an overall severity score to each based on the Fazekas scale, ranging from 0 to 3. Montreal Cognitive Assessment (MoCA) scores were used as a measure of cognitive function. Patients with confounding diagnoses were excluded. Multiple regression analyses were conducted between WMH and cognitive scores, adjusting for hypertension, diabetes and smoking.
Results:
Multiple regression models revealed R2 values of 0.097, 0.050 and 0.036 for overall, PV and SC WMH with MoCA, respectively. There were negative associations between overall Fazekas scores and MoCA (B = −2.11, p < 0.001), PV scores and MoCA (B = −1.46, p < 0.001) and SC scores and MoCA (B = −1.21, p = 0.002).
Conclusion:
The association between MRI WMH and cognition supports prognostic use for cognitive decline to limit/delay deterioration. Specifically, stronger PV associations prompt research and perhaps development of revised scales prioritizing PV changes. Implementing this into the field of radiology whereby WMH severity and location assessment becomes a standard within brain MRI reports could improve patient outcomes.