Neuropsychological batteries utilized in MS patients.
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More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
\n'}],latestNews:[{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"}]},book:{item:{type:"book",id:"2151",leadTitle:null,fullTitle:"Novel Approaches and Their Applications in Risk Assessment",title:"Novel Approaches and Their Applications in Risk Assessment",subtitle:null,reviewType:"peer-reviewed",abstract:"Risk assessment is a critical component in the evaluation and protection of natural or anthropogenic systems. 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His research interests include numerical modeling for unsteady-state biogeochemical processes of chemical transport in complex environmental systems, GIS technologies in hydrologic simulation, environmental assessment, and watershed management, integrated risk assessment for human health and ecosystem at watershed scales, impact of water resources and global climate change on hydrology, environmental quality, and crop production.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"University of California, Davis",institutionURL:null,country:{name:"United States of America"}}}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"780",title:"Ecological Engineering",slug:"ecological-engineering"}],chapters:[{id:"35499",title:"A Practical Example of Risk Assessment – Risk Assessment to Phycotoxins in a Recreational Shellfish Harvester’s Subpopulation",doi:"10.5772/38017",slug:"a-practical-example-of-risk-assessment-risk-assessment-to-phycotoxins-in-a-recreational-shellfish-ha",totalDownloads:1514,totalCrossrefCites:1,totalDimensionsCites:4,signatures:"Cyndie Picot and Alain-Claude Roudot",downloadPdfUrl:"/chapter/pdf-download/35499",previewPdfUrl:"/chapter/pdf-preview/35499",authors:[{id:"115208",title:"Prof.",name:"Alain-Claude",surname:"Roudot",slug:"alain-claude-roudot",fullName:"Alain-Claude Roudot"},{id:"118204",title:"Dr.",name:"Cyndie",surname:"Picot",slug:"cyndie-picot",fullName:"Cyndie Picot"}],corrections:null},{id:"35500",title:"Spatial Cadmium Distribution in the Charente Watershed and Potential Risk Assessment for the Marennes Oleron Bay (Southwest France)",doi:"10.5772/38897",slug:"spatial-cadmium-distribution-in-the-charente-watershed-and-potential-risk-assessment-for-the-marenne",totalDownloads:1527,totalCrossrefCites:0,totalDimensionsCites:0,signatures:"Coynel Alexandra, Khoury Alaa, Dutruch Lionel, Blanc Gérard, Bossy Cécile, Derriennic Hervé and Schäfer Jörg",downloadPdfUrl:"/chapter/pdf-download/35500",previewPdfUrl:"/chapter/pdf-preview/35500",authors:[{id:"120815",title:"Dr.",name:"Alexandra",surname:"Coynel",slug:"alexandra-coynel",fullName:"Alexandra Coynel"},{id:"120915",title:"Prof.",name:"Gérard",surname:"Blanc",slug:"gerard-blanc",fullName:"Gérard Blanc"},{id:"120968",title:"Mr.",name:"Alaa",surname:"Khoury",slug:"alaa-khoury",fullName:"Alaa Khoury"},{id:"120970",title:"Dr.",name:"Lionel",surname:"Dutruch",slug:"lionel-dutruch",fullName:"Lionel Dutruch"},{id:"120972",title:"Mrs.",name:"Cécile",surname:"Bossy",slug:"cecile-bossy",fullName:"Cécile Bossy"},{id:"120973",title:"Mr.",name:"Hervé",surname:"Derriennic",slug:"herve-derriennic",fullName:"Hervé Derriennic"},{id:"145744",title:"Prof.",name:"Jörg",surname:"Schäfer",slug:"jorg-schafer",fullName:"Jörg Schäfer"}],corrections:null},{id:"35501",title:"Planning and Decision Support Tools for Integrated Water Resources Management (IWRM) on River Basin Level in the Southeast-Asian Region on the Example of Vietnam - 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\r\n\tThis book is devoted to discussing several topics on quantum information science. Studying this subject, we see its consequences are related to quantum effects in physics. We realize that quantum theory and the interpretation of quantum mechanics are responsible for various theoretical progress and experimental topics, visioning quantum devices' implementation. However, the understanding of quantum physics and engineering is a serious challenge to solve. In the last decade, quantum information science development is considerable compared to before two decades ago, or more, and some remarkable progress in manufacturing quantum computers are observed recently. The discussion of topics related to quantum information science is now crucial. For this reason, several efforts made to discuss topics addressed from the fundamentals to applications is relevant. In the current issue, theoretical background and other topics such as quantum communication, quantum algorithm, other applications as quantum complexity, and physical implementations, including other quantum information topics, are welcome.
",isbn:"978-1-83968-769-3",printIsbn:"978-1-83968-768-6",pdfIsbn:"978-1-83968-770-9",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,hash:"d7481712cff0157cd8f849cba865727d",bookSignature:"Prof. Sergio Curilef and Dr. Angel Ricardo Plastino",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10674.jpg",keywords:"Quantum Computers, General Theorems, Quantum Cryptography, Teleportation, Quantum Fourier Transform, Quantum Walk Models, Machine Learning, Quantum Turing Machines, Quantum Computation, Quantum Optics, Artificial Intelligence, Quantum Simulation",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"February 1st 2021",dateEndSecondStepPublish:"March 1st 2021",dateEndThirdStepPublish:"April 30th 2021",dateEndFourthStepPublish:"July 19th 2021",dateEndFifthStepPublish:"September 17th 2021",remainingDaysToSecondStep:"3 days",secondStepPassed:!1,currentStepOfPublishingProcess:2,editedByType:null,kuFlag:!1,biosketch:"A pioneering researcher in Statistical Physics of Nonequilibrium in the north of Chile.",coeditorOneBiosketch:"Researcher on the multidisciplinary application of ideas and techniques inspired by information theory.",coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"125424",title:"Prof.",name:"Sergio",middleName:null,surname:"Curilef",slug:"sergio-curilef",fullName:"Sergio Curilef",profilePictureURL:"https://mts.intechopen.com/storage/users/125424/images/system/125424.jpeg",biography:"Sergio Curilef has been a full professor in the Physics Department, Universidad Católica del Norte, Antofagasta, Chile, since 1998. He obtained his Ph.D. in Physics from the Brazilian Center for Research in Physics (CBPF)-RJ, Brazil, in July 1997. \nHis main research interests are statistical physics and quantum mechanics of systems with long-range interactions, particles in magnetic fields, and nonlinear phenomena. He has recently developed research on complex systems and applications to science and engineering. He is the principal investigator in several research projects, and he did a sabbatical year at the University of Pretoria, South Africa, in 2007. He has also created the undergraduate and postgraduate programs in Physics at his university, where he is currently director of the Physics Department.",institutionString:"Universidad Católica del Norte",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"4",totalChapterViews:"0",totalEditedBooks:"1",institution:null}],coeditorOne:{id:"340548",title:"Dr.",name:"Angel",middleName:"Ricardo",surname:"Plastino",slug:"angel-plastino",fullName:"Angel Plastino",profilePictureURL:"https://mts.intechopen.com/storage/users/no_image.jpg",biography:"Angel Ricardo Plastino is Professor at the Departamento de Ciencias Básicas de la Universidad Nacional del Noroeste de la Provincia de Buenos Aires (UNNOBA), Argentina. He has a Ph.D. in astronomy from the Universidad Nacional de La Plata, Argentina. The main research interests of Prof. A. R. Plastino are centered on the multidisciplinary application of ideas and techniques inspired by information theory. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"66214",title:"Neuropsychological Functions and Cognitive Neurorehabilitation in Multiple Sclerosis",doi:"10.5772/intechopen.85511",slug:"neuropsychological-functions-and-cognitive-neurorehabilitation-in-multiple-sclerosis",body:'Historically the disease today known as multiple sclerosis (MS) has been referred to in the historical medical literature with a variety of terms, including, disseminated sclerosis and sclerose en plaque [1]. Lidwina van Schiedam, was the first potential case of MS dating as far back as 1421, when Jan van Berieren commented on her illness. Records showed that she had difficulties walking, paralysis of the right arm, decreased sensation and visual difficulties [2].
Today we know that MS is a chronic inflammatory autoimmune degenerative disease of the central nervous system (CNS). It is the most common non-traumatic neurological disorder among young adults leading to disability. The etiology of MS involves white matter pathology, cortical atrophy, cortical lesions, and microstructural abnormalities in deep gray matter that impact structural and functional connectivity [3]. Cognitive impairment in MS appears to be a result of this diffuse disruption in brain networks [4]. These patients may also present sensorimotor [5], visual [6], bladder, cerebellar [7] and emotional difficulties leading to functional disability [8] and poorer quality of life [9].
Environmental factors and especially geographical latitude may significantly influence the development of MS. However, genetic susceptibility as is evident from twin studies and familial cases, suggests that MS disease causality is due to a complex interaction between multiple genes and environmental factors, eventually leading to inflammatory-mediated central nervous system deterioration [10]. Genomic studies, with specific HLA antigens (HLA-DR2), have confirmed the genetic susceptibility of MS [10]. Numerous other environmental factors have been evaluated that may be associated with MS, but methodological caveats have casted doubts on their validity. On average, MS patients contracted common childhood illnesses at later ages than healthy controls [11]. A biomarker of Epstein-Barr virus (anti-EBNA IgG seropositivity), infectious mononucleosis, and smoking have shown the strongest consistent evidence of an association. However, additional data and better-designed studies are needed to establish robust evidence [12].
MS disease course is heterogeneous in nature and several types have been described: Relapsing remitting MS (RRMS), Active (with relapses and/or new lesions on MRI), Not Active (no relapses or MRI activity), Progressive MS (Secondary Progressive MS (SPMS) and Primary Progressive MS (PPMS), Active with Progression (relapses/MRI activity and clinical deterioration not due to relapses), Active but without Progression (relapses but no clinical deterioration), Not Active but with Progression, Not Active and without Progression (stable disease) [13]. The use of these terms is primarily for descriptive purposes and for setting reasonable expectations for treatment.
This chapter is not a comprehensive review of the extensive literature on neuropsychological functions and cognitive rehabilitation in multiple sclerosis, but rather a selective review of the most relevant features related to this topic.
Dating back to the seminal writings on MS, Charcot’s observations of the adverse effects that MS exerts on memory, concept formation, and the intellect [14], were underestimated for many decades in the neurology literature. It was only with the emergence of the comprehensive care model in the early 1980s, that the nature and significance of cognitive dysfunction in MS became appreciated. The medical community, due to the often-subtle nature of cognitive deficits in MS, and the difficulty in detecting these deficits during routine clinical practice, was initially slow to appreciate them as a core clinical symptom of MS. Instead, they believed that cognitive impairment was a relatively rare entity in MS, occurred only in advanced cases with a high level of physical disability and was associated with subcortical dementia [15].
Cognitive difficulties are not frequently reported by patients among the initial symptoms of MS, although there is sufficient evidence that cognitive impairment is present from the early stage of the disease (see for e.g., the study by [16], which assessed MS patients neuropsychologically, not more than 2 years after experiencing their first neurological symptoms, and [17], who presents three cases evaluated at different stages of the disease). Moreover, cognitive impairment may be present in the early stages of the disease in patients with relatively low or mild physical disability (see for e.g. the studies by [18, 19] who found cognitive deficits in patients with an EDSS disability score of ≤3.5, that had not yet been influenced significantly in their daily functional abilities and employment status). A recent anatomofunctional study utilizing diffusion imaging and resting state functional MRI, revealed that disconnection in the default mode network (DMN) and attentional networks (ATT), may deprive the brain of the necessary compensatory mechanisms required to face the widespread structural damage during the early course of MS, providing a possible explanation for the cognitive dysfunction in these early stages of the disease [20].
Although it is now commonly accepted that roughly one-half of individuals with MS [21, 22], will experience clinical deficits over the course of the disease, prevalence rates are highly variable and depend to a large extent on the type of MS population studied, the clinical, demographic and sociodemographic characteristics and the year conducted. A recent study that included RRMS and SPMS patients attending an outpatient neurology clinic reported an overall cognitive dysfunction prevalence rate of 53.7% [23]. Moreover, the study by [22], reported that 47% of their MS patients recruited from an outpatient clinical setting, diagnosed with the revised McDonald criteria [24], the majority with RRMS and mean duration of illness at 9.6 years, assessed with a brief cognitive measure (BICAMS), performed below the 1SD cutoff set for impairment on at least one of the three tests that comprise this brief neuropsychological battery. In an interesting cross-sectional study that evaluated the patterns of cognitive impairment in patients with disease duration of up to 30 years, 20.9% performed below the 1SD cutoff for impairment by the 5th year from disease onset, by 10 years this had reached 29.3%. By utilizing regression modeling the authors suggested that cognitive impairment may precede MS onset by 1.2 years [25].
Most of the evidence suggests that cognitive impairment in MS patients is present during all disease stages and across all disease clinical subtypes [26, 27, 28], including, RRMS, PPMS, SPMS, Clinically Isolated Syndrome (CIS) and “benign MS” [29, 30], and even Radiologically Isolated Syndrome—(RIS) [31]. Based on the majority of studies that have compared cognitive functions across disease subtype, deficits appear to be more frequent and more widespread in the progressive type rather than in the relapsing form of the disease [23, 29, 31, 32].
The dissemination of lesions in cerebral white matter including their affinity for periventricular regions provides the basis for some cognitive dysfunction commonalities [33]. In this respect, some cognitive domains appear to be more commonly compromised than others. Information processing efficiency, episodic memory, attention, and executive functioning are the domains found predominantly to be detrimentally affected in MS [21, 34, 35]. Among these domains the most common pattern involves circumscribed deficits as a combination of one or two of the above-mentioned domains (e.g., attention/processing speed, learning/memory, and or executive functions [11, 15, 21].
Symptoms like cognitive and physical fatigue, which are often accompanied by depression and anxiety, may negatively influence cognition in MS patients. This is especially true when extended periods are required to complete and appear more relevant for the patient’s daily life than what may be assumed by many physicians treating MS patients [11].
Although cognitive impairment is highly prevalent among MS patients, some have a tendency to withstand severe disease burden (e.g., white matter lesions and cerebral atrophy), and present with overall lower levels of cognitive decline. One possible explanation for this protective mechanism is the brain reserve hypothesis and the cognitive reserve theory [36]. Recently, it has been verified that highly significant protection for cognitive impairment is provided by brain reserve, defined as the maximal lifetime brain growth (MLBG), and estimated with intracranial volume or head circumference. Larger MLBG a proxy for neuronal and synaptic count has been linked to lower risk for cognitive impairment in MS [37]. This larger MLBG appears to be associated with more robust neural networks resistant to disease-related disruption and also provides more potential degrees of freedom for the brain to plastically reorganize in the face of MS disease related challenges.
The multidimensional nature of cognitive dysfunction in MS necessitates an assessment of numerous cognitive domains. The challenge until recently was to find the optimal combination of cognitive tests that would provide an accurate picture of the deficits whilst avoiding the use of unnecessary and time-consuming measures [15].
In order to overcome some of the limitations in assessing cognition in MS, and considering the fact that not all neuropsychological measures are appropriate for the MS population, a number of neuropsychological assessment tools (brief screening batteries and comprehensive neuropsychological batteries), have been utilized specifically for this population in routine clinical care and for research purposes. Table 1 provides a summary of the most important neuropsychological tools utilized in MS patients.
Cognitive domain | Rao brief repeatable neuropsychological battery (BRB) | Minimal assessment of cognitive function in MS (MACFIMS) | NINDS common data elements | Brief assessment of multiple sclerosis (BICAMS) |
---|---|---|---|---|
Cognitive processing speed | SDMT | SDMT | SDMT | SDMT |
PASAT | PASAT | PASAT | — | |
Language | COWAT | COWAT | COWAT | — |
Visual/spatial | — | JLO | — | — |
Memory | SRT | CVLT2 | CVLT2 | CVLT2 |
10/36 Spatial Recall Test | BVMTR | BVMTR | BVMTR | |
Executive function | — | D-KEFS | D-KEFS | — |
Neuropsychological batteries utilized in MS patients.
SDMT: Symbol Digits Modalities Test; PASAT: Paced Auditory Serial Addition Test; COWAT: Controlled Oral Word Association Test; CVLT2: California Verbal Learning Test 2nd edition; BVMTR: Brief Visuospatial Memory Test Revised; DKEFS: Delis Kaplan Executive Function System Sorting Test.
Although MS was originally considered to be a disease of White Matter (WM), more recently with the development and utilization of advanced immunohistochemistry techniques investigators have begun to appreciate that demyelination of gray matter (GM) is a common neuropathological feature in MS patients. Demyelination of GM appears to be more common in the cerebellum, spinal cord and hippocampus. Essentially, however, no areas within the CNS are actually spared [38]. The thalamus is considered the most frequently affected subcortical GM structure, but lesions have been identified within the putamen, pallidum, caudate, amygdale, substantia nigra and hypothalamus [39].
Considering the above, clinicians and researchers investigating neuropsychological functions in MS patients have realized that cognitive dysfunction in this population cannot be explained by WM pathology alone. GM pathology appears to have a significant impact on cognitive impairment, but requires novel neuroimaging technology in order to detect and visualize these types of lesions. Due to these visualization difficulties in current imaging technologies, research in MS has shifted its focus primarily to comparing WM and GM measures of atrophy [39]. In this respect, [40], noted a similar increase in WM atrophy across disease stages (three-fold), whereas, atrophy of the GM increased proportionally according to disease stage, i.e. three-fold in CIS converting to RRMS, versus 14-fold in SPMS patients.
Another important issue is that GM atrophy has been reported to be regionally specific, involving early volume loss of the basal ganglia, corpus callosum and thalamus. Recent studies have outlined the significance of thalamic volume in relation to cognitive impairment. One such report by [41] found lower thalamic volumes in MS patients compared to healthy participants, with the lowest volumes found in severely cognitive impaired patients. In one of our recent studies, we provide evidence that thalamic atrophy was the best predictor of cognitive dysfunction in RRMS patients and was also highly associated with activities of daily living and employment status [42]. Moreover, in a similar study that recruited late stage SPMS patients, we found that corpus callosum atrophy was associated with deficits in cognitive flexibility, processing speed, episodic memory, executive functions, reaction time and phonological verbal fluency. Processing speed and composite memory were the most sensitive markers for predicting employment status. Corpus callosum atrophy was the most sensitive MRI marker for episodic memory and processing speed deficits. Moreover, corpus callosum atrophy predicted a clinically meaningful cognitive decline, affecting employment status in our SPMS patients [43]. Thus, it appears that irreversible tissue loss, as measured by brain atrophy of the white and gray matter, is strongly associated to cognitive function in the MS population. While white matter atrophy has also been reported to contribute significantly to impairment in mental processing speed and working memory, gray matter atrophy was highly predictive for verbal memory status, but additionally predicted neuropsychiatric symptoms such as disinhibition and euphoria [44].
Recent evidence from empirical research has indicated that cognitive dysfunction in MS patients is highly related to everyday functioning abilities [45]. One such study that evaluated associations between cognitive functions and objective performance on measures of everyday functioning in MS, [46], reported that MS patients had significantly more difficulties in simple and more complex cooking abilities, using the phone, taking medication, and paying the bills, compared to healthy participants. An interesting study by O’Brien et al. [47] and a more ecologically valid study by Goverover et al [48], utilizing an actual reality (AR) approach through the use of everyday tasks requiring the internet (e.g. booking an airline ticket, purchasing cookies and ordering pizza), the authors report significant correlations between these tasks and performance on mental processing speed (SDMT), concluding that this measure contributes significantly to predicting everyday functioning capacity in MS. A more recent study, [48], examined the ability of MS patients to manage their finances. The authors found that MS patients demonstrated and reported more difficulties in managing their finances compared to healthy controls. Moreover, MS patient’s difficulties in handling their finances were associated with the severity of cognitive dysfunction. As this important everyday task requires intact mental processing ability and executive-attentional abilities, domains usually impaired in MS individuals, these findings may serve as potential intervention indicators when planning cognitive rehabilitation interventions.
From the findings reported by the studies mentioned previously, it becomes obvious that interventions to alleviate, stabilize, reduce or compensate for cognitive impairment are of an extremely high priority, in order to provide MS individuals with the necessary mechanisms to better handle their everyday functioning disabilities. The evidence up till now is only modest regarding the efficacy of pharmacological agents on cognitive dysfunction [49, 50], and non-pharmacological interventions such as cognitive rehabilitation also provide incomplete evidence on whether they might improve or stabilize cognitive impairment and especially over long follow up periods [51]. Despite this general consensus, there are studies that have reported the efficacy of pharmacological agents [52] and cognitive rehabilitation [28, 53, 54] in reducing MS associated cognitive deficits.
The goals of non-pharmacological treatments for MS-related cognitive deficits are similar to those of the immune-modulating drugs. In other words, these interventions are used with the intent of preventing the progression of cognitive dysfunction and promoting a therapeutic ‘milieu’ in which optimal cognitive functioning can occur, and include specific approaches which are known to be effective in remediating cognitive disorders of any etiology [15]. Cognitive rehabilitation or ‘rehabilitation of individuals with cognitive impairment’ [55] include specific approaches designed to assist the MS patient to better cope with existing cognitive impairments or to improve a specific cognitive skill. It focuses on two main approaches: the restorative or functional training approach (i.e. ameliorating patients’ deficits in processing and interpreting information—e.g. when cognitive training is used to enhance attention or memory performance). The restorative approach depends on the brains capability of cortical reorganization following injury (i.e. that the brain possesses some degree of plasticity). The second is the compensatory or strategy training approach (e.g. modifying the patient’s environment, using a calendar and set phone reminders). These approaches have different goals and limitations, and may be used in isolation or in combination. For example, in patients with extensive tissue loss, neural plasticity might be hampered and no or little effect will result from restorative or functional training. In that particular patient, compensatory or strategy training might help the patient to work around the problems that are present. As for most MS patients, especially those with a relapsing disease course, it is expected that restorative or functional training will lead to improved cognitive functioning on neuropsychological measures, improved functioning in everyday life activities, and ultimately will lead to an improvement in network efficiency [56].
Several studies have investigated the effectiveness of cognitive rehabilitation interventions in patients with MS, including computer-based training and neuropsychological counseling, but with inconsistent results. The majority of studies found improvements in specific cognitive domains, but the evidence provided in the literature remains inconclusive [57]. A significant limitation in providing evidence on the efficacy of studies involving cognitive rehabilitation is the great variability in the methods or strategies utilized for treatment, the measures used to assess cognition and other secondary outcome variables and the lack of ecologically valid outcome measures in order to assess the efficiency of these interventions in everyday functioning ability.
Applying a technique known as the Story Memory Technique (SMT), [58] provided class 1 evidence that this technique applied for 5 weeks/twice weekly (10 sessions) with an emphasis on teaching context and imagery to facilitate learning, improved episodic memory in MS patients relative to controls and moreover produced increased f-MRI activation during a memory task in frontal and parietal regions. Positive effects were additionally observed for objective measures of everyday memory function, general contentment, and executive functioning. These positive outcomes were sustained for a period of 6 months.
Clinical trials utilizing the RehaCom computerized software in MS patients with cognitive impairments have also shown positive outcomes. Bonavita et al. [59], noted significant pre-to post treatment improvements in a RehaCom treated MS cohort, on mental information processing, executive functions and attention. This and other similar studies have reported positive outcomes in MS patients treated with this software, and moreover, associations between functional neuroimaging (f-MRI) findings with changes in neurocognitive measures have been reported [59, 60, 61]. In a multicenter Italian study, RehaCom was utilized to provide specific intensive cognitive training for 12 months. Results showed that MS patients treated with this modality had improved scores post treatment on the SDMT, PASAT, and episodic memory measures relative to MS patients who received aspecific psychological therapy for the same period of time [62].
In 2017, our group, [53], conducted a multicenter randomized controlled trial with 58 clinically stable RRMS patients utilizing computer-assisted (RehaCom) functional cognitive training with an emphasis on episodic memory, information processing speed/attention, and executive functions for 10 weeks. Our findings revealed that only the group that had received functional cognitive training showed significant improvements in verbal and visuospatial episodic memory, processing speed/attention, and executive functioning from pre—to postassessment. Moreover, the improvement obtained on attention was retained over 6 months providing evidence on the long term benefits of this intervention. Treated patients rated the intervention positively and were more confident about their cognitive abilities following treatment.
While the previously mentioned positive results regarding the efficacy of cognitive rehabilitation interventions in MS individuals cannot be overstated, it is important to note that a recently published Cochrane Review that included 15 studies and 989 MS participants regarding the efficacy of memory retraining techniques with or without the assistance of computer software, concluded that there is only limited evidence on the effectiveness of memory rehabilitation in this population. The authors further suggest that more RCTs of high methodological quality be conducted with the utilization of ecologically valid outcome assessments [63].
Another Cochrane Review that included 20 studies and 966 MS participants evaluating the effectiveness of neuropsychological rehabilitation in MS [64], reported low-level evidence for the positive effects of neuropsychological rehabilitation in this population. However, the authors reported that the comparability of the 20 studies reviewed was limited due to heterogeneity of interventions and outcome measures. It should be noted however, that the majority of studies included in this review did show some evidence of positive effects on cognitive outcome measures.
Despite the limitations noted by the previously mentioned Cochrane reviews, a growing body of literature supports the efficacy of cognitive rehabilitation for individuals with MS and more randomized controlled trials are needed to support existing and new rehabilitation techniques. Cognitive rehabilitation appears to be useful for all patients with MS regardless of disease course and level of cognitive impairment, although studies including exclusively MS patients with progressive disease course are limited. Future clinical trials utilizing cognitive rehabilitation interventions in progressive MS patients should become a priority.
Cognitive impairment is frequently encountered in MS individuals, irrespective of disease duration, severity of physical disability, and at both the earlier and later disease stages. Moreover, cognitive dysfunction in this population may have a significant negative impact on quality of life, activities of daily living and employment status. Furthermore, past and current pharmacological treatments have shown inconsistent findings in alleviating cognitive impairment in individuals with MS requiring further clarification. This inconsistency regarding the effects of pharmacological interventions on cognition, coupled with the reduced ability to effectively handle everyday tasks, loss of employment and social interaction capacity, prioritizes the need for utilizing potentially more effective non-pharmacological, neurobehavioral interventions to address cognitive dysfunction and everyday functioning abilities. Neurobehavioral interventions utilizing cognitive rehabilitation have shown favorable effects on MS patients cognitive performance and other related skills, and in some cases, have managed to generalize these positive effects to MS individual’s everyday life functioning ability. In this respect it becomes obvious that there is a need for rigorous new cognitive neurorehabilitation studies that may overcome some of the methodological limitations of older studies, and provide robust evidence regarding the efficiency of such cognitive interventions for the MS population.
The authors have no conflict of interest.
Parts of this chapter originate from my Doctoral Dissertation entitled: Neuropsychological functions and association with Single Photon Emission Computed Tomography (SPECT) in Greek Multiple Sclerosis patients: Efficacy of a Computerized Cognitive Rehabilitation Intervention (2017). Department of Neurology, University of Patras Medical School, Patras, Greece.
In the era of antibiotics, vaccines and other medical innovations, life expectancy has increased worldwide, which has led to an enhanced prevalence chronic diseases. Only in the USA, the Department of Health and Human Services estimates that by the year 2040, 82.3 million Americans (21.7% of the population) will be over 65 years of age [1]. Consequently, age-related illnesses that cause a significant morbidity and mortality will become a rising public health problem. At the same time, there is an increase in the prevalence of multimorbidity, defined by the coexistence of two or more chronic pathologies in the same individual. Studies show that in individuals that are over 60 years old, the multimorbidity range is from 55 to 98% [2]. Multimorbidity is associated with functional decline, disability, poor quality of life, higher emergency care and hospitalizations rates, polypharmacy and increased healthcare costs, all of which are a great burden for society [3].
\nThe concept of cognitive impairment has been carefully analysed in the last two decades, given the devastating consequences of this problem, mainly among elderly populations. Cognitive function can be divided into six large domains: language (verbal fluency and comprehension), learning ability and memory (work memory and memory-based tagging), attention, executive functions (planning and problem solving), praxis (motor-ideative, ideative and visual constructive) and visuospatial function [4].
\nMild cognitive impairment (MCI) is defined as a cognitive dysfunction more severe than normal age-related cognitive decline or education level, but not severe enough to significantly interfere with daily function [5]. MCI exceeds the “age-related” decline in cognition healthy individuals experience but does not meet the criteria for dementia. Furthermore, not all cases of MCI will progress towards dementia.
\nIn the general population, studies have shown a prevalence of MCI between 10 and 20% in older adults [5]. However, cognitive impairment is heavily underdiagnosed and undertreated by primary care physicians. There are several screening tools that can identify those with a high risk of MCI such as the Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Saint Louis University Mental Status Examination (SLUMS) or Rapid Cognitive Screen. Once the diagnosis of cognitive dysfunction is determined, it is essential to establish the aetiology and the contributing factors and to evaluate if there are any reversible causes. Every practitioner should be familiar with these questionnaires, especially MMSE, and should use them whenever they suspect a person of MCI.
\nNeuroanatomical structures and their function can be assessed by neuroimaging techniques. Computed tomography (CT) scan and magnetic resonance imaging (MRI) can analyse the brain structure and exclude conditions such as strokes, brain tumours or vascular malformation. The fluorodeoxyglucose positron-emission tomography (FDG-PET) scan, mostly used for research purposes, can evaluate the brain function and seems to be more sensitive than MRI in MCI diagnosis. This tool uses a radioactive glucose tracer which binds to highly active brain areas. The presence of hypometabolic areas in the temporal or parietal lobe is a sign of neurodegeneration. Subjects who develop these hypometabolic areas have a higher risk of progression from MCI to dementia [6, 7]. For research purposes, there are several biomarkers used for the diagnosis of MCI and dementia, but the lack of standardization regarding optimal cutoff points limits their clinical utility [8].
\nThere are well-established risk factors for developing MCI: age, male gender, family history of cognitive impairment, the presence of the apolipoprotein E allele, smoking and low educational level [9]. Moreover, one study, which aimed to determine if multimorbidity could be a risk factor for mild cognitive impairment and dementia, found that individuals who associate at least two of the following, hypertension, hyperlipidemia, coronary artery disease and arthritis, had a very high risk of MCI [3].
\nRecent studies showed that some chronic respiratory conditions, such as chronic obstructive pulmonary disease (COPD), obstructive sleep apnea (OSA) or idiopathic pulmonary fibrosis (IPF), have an important impact on cognitive function. There are discrepancies regarding the reported prevalence of cognitive dysfunction among the conditions listed above, which can be explained by study design and limitations: diagnostic methods for cognitive impairment (psychometric tools or neuroimaging), small sample size or inappropriate control group, assessment moment (stable phase/exacerbation), the severity of the airflow limitation, presence of hypoxia and the use of long-term oxygen therapy. Multiple confounders can also contribute to the large variation of data regarding prevalence: age, education level, smoking history, comorbidities, etc.
\nSleep apnea syndrome is a disorder of breathing during sleep, characterized by total or partial obstruction of the upper airways leading to hypoxia and hypercapnia, plus increased respiratory effort [10]. These features produce micro-awakenings that result in disruption of sleep and changes in neuronal activity. All of these are potential mechanisms for cognitive deficiency [11].
\nIn adults, the prevalence of OSA increases significantly with age. Between 30 and 49 years, 10% of men and 3% of women are diagnosed, increasing to 17 and 9%, respectively, for 50–70 years [12] and with increasing prevalence among postmenopausal women [13]. These percentages are higher than those published 10 years ago, due to the fact that obesity is increasing among the population of developing countries [14]. More worryingly, the true prevalence may be underestimated as many people with OSA remain undiagnosed.
\nNighttime symptoms are noisy snoring, non-restful sleep, nocturia, sweating and dry mouth. One of the most common daytime symptoms in patients with OSA is daytime sleepiness. This greatly influences the quality of life and cognitive performance.
\nOSA has been associated with a wide range of psychological problems such as depression, anxiety, neurocognitive dysfunction, especially attention, alertness, memory and learning, phenomena due to fragmentation of sleep and intermittent hypoxemia [15, 16, 17]. Fragmentation of sleep, sleep deprivation and the association of excessive daytime sleepiness are proposed mechanisms that underlie cognitive impairment through their impact on attention [18, 19].
\nThe exact prevalence of cognitive disorders and their severity due to multiple comorbidities with which this syndrome is associated is not known in adult patients with OSA.
\nThere are numerous OSA comorbidities that can influence cognitive function, such as treatment-resistant hypertension [20], diabetes [21], COPD, congestive heart failure, strokes [22], smoking [23] and alcoholism [24]. Also age, sex (male), obesity and the use of psychoactive drugs are considered independent risk factors [25].
\nAgeing itself causes decline in cognitive function, and the presence of OSA in these patients leads to further brain injury, with cognitive impairment being more obvious [26]. It is also known that smoking, through its damaging effects on blood vessels and circulation, increases the risk of dementia, both vascular and Alzheimer’s, as well as neurocognitive decline not associated with dementia [27].
\nAnother important factor in the association of OSA with cognitive decline is, it seems, the genetic factor. Thus, studies show that the presence of apolipoprotein E4 (ApoE4) is associated with an increased incidence of cognitive disorders [28].
\nHigh blood pressure is associated with cognitive decline, both when isolated and in the presence of metabolic syndrome, especially due to the presence of cardiovascular risk factors [29].
\nAlso, the presence of hypothyroidism in patients with OSA may accelerate cognitive decline, and current data are not sufficient to demonstrate whether the treatment ameliorates the decline phenomena [30].
\nModerate alcohol consumption may protect against dementia, but significant alcohol consumption is associated with cognitive impairment, which is manifested by loss of memory, impaired personality and impaired judgement [24]. Alcohol intake before bedtime affects sleep architecture [31]. In addition, depending on the quantity, the instability of the upper airways may increase [32]. Thus, excessive alcohol use by patients with OSA may lead to more severe cognitive deficits.
\nAnother common comorbidity of OSA is stroke, which, independently, is accompanied by a cognitive deficiency and even dementia. Studies show that up to 30% of patients with stroke can develop dementia [33, 34]. And psychoactive medication, e.g. benzodiazepines, narcotics and barbiturates, can aggravate OSA and increase attention and alertness problems [35, 36].
\nStudies carried out over time have shown structural and functional changes in the brain, resulting in cognitive deficiency. There are studies that, by MRI techniques, have shown decrease of grey matter in the hippocampus; cerebellum; frontal, parietal and temporal lobes; as well as the anterior cingulate cortex [37, 38, 39]. Also, a decrease in the hippocampus was observed, which plays an important role in memory consolidation. The white matter changes reported by O’Donoghue et al. indicate that axonal or glial pathology is also present in OSA, consistent with other previous findings [40].
\nStudies on the cardiovascular effects of OSA have shown that the disorder results in changes in vascular structure and function, these changes being frequently encountered in other hypoxic populations [41]. It is assumed that hypoxia would have a direct effect on the neuropsychic in patients with OSA, with existing similar mechanisms in terms of cardiovascular changes and brain vessels. Hypoxia produces immediate vasodilation, being a protective mechanism to more efficiently distribute oxygen to the affected organ. Studies have shown that this protective mechanism does not exist in patients with OSA [42]. One potential reason why these patients do not have a response to hypoxemia is because they suffer from repeated episodes of hypoxemia (over five events/h) and desaturation, not just a sustained hypoxic event. Thus, the post-episode recovery time being limited, it is not possible to estimate whether there is a protective response to recurrent hypoxic events, but it is assumed that the vessels would suffer [43].
\nTherefore, in patients with OSA, there are lesions due to hypoxia and reperfusion with increased lipid peroxidation. This process involves the oxidation of polyunsaturated fatty acids with the formation of reactive oxygen species and toxic products, having potential damaging effects for the brain and heart.
\nAlso, in patients with vascular pathology, endothelial dysfunction is present. In patients with OSA, imbalances between vasoconstrictive mediators (higher thromboxane and endothelin levels) and vasodilators (nitric oxide, prostacycline) appear, and nitric oxide production has been shown to decrease in OSA. This imbalance predisposes to atherosclerosis [44]. Thus, the effects on cerebral flow, as well as hypoxia, may cause the onset of cerebral infarctions, resulting in vascular dementia. The presence of endothelial dysfunction, with the onset of neurocognitive deficits, has been described even in studies performed in the paediatric population [16].
\nThere are authors who consider that the cognitive impairment in OSA represents the short-term consequence of the poor quality of sleep manifested by daytime sleepiness or attention difficulties. Studies have shown specific and localized frontal lobe involvement, responsible for the executory dysfunction observed in OSA [45]. The basis of this hypothesis is that sleep disruption reduces the efficiency of restoration processes in the prefrontal cortex that will also lead to cellular and biochemical stress. These processes, in turn, disrupt functional homeostasis, altering the viability of neuronal and glial cells [46, 47, 48]. The severity of sleep fragmentation is associated with attention deficit and decreased alertness, and the overall cognitive deficit is the consequence of hypoxia. Due to sleep fragmentation, alteration of blood gases and changes of homeostasis in the frontal lobe and hippocampus leads to memory impairment and executory function deficiency.
\nA direct consequence of OSA, with impact on both personal and social levels, is the loss of vigilance. This increases the risk of traffic accidents in untreated patients, which is why it is important to diagnose and treat this condition as early as possible [49]. Election treatment of OSA is continuous positive airway pressure (CPAP) therapy. This method was first described in 1981 [50]. Since then, technological progress has been made to suit the needs of patients. Also, in order to improve treatment adherence, device manufacturers have considered the importance of producing mask interfaces that match the user’s physiognomy. This variety improves comfort and reduces air leakage. The use of CPAP for at least 4 h of sleep during a 24-h period defines a minimum acceptable level in terms of a beneficial therapeutic response. Thus, for maximum benefit, most clinicians recommend using the device for the entire duration of sleep [51].
\nCanessa et al. studied the effects of CPAP therapy on neurocognitive changes in 17 OSA patients. Therefore, voxel-based morphometry determinations showed significant post-therapy improvements in the cognition level, together with the increase of the volume of the grey matter in the frontal lobe and hippocampus [52]. This is why early diagnosis and initiation of CPAP therapy could prevent, in the medium and long term, the cognitive impairment. In summary, this study provides the first evidence that structural brain abnormalities exist in hypoxemia-sensitive regions and they may change with treatment. These results suggest that even the negative neurological effects of hypoxemia can be reversed with consistent and complete treatment. Therefore, adherence to CPAP treatment can lead not only to clinical recovery but also to structural brain recovery. It should be noted that the patients in this study showed a positive response to treatment. MRI may thus be used as a marker, to evaluate the response to treatment [53].
\nThere are studies that show that use of CPAP over 12 months also leads to significant recovery of the impaired white matter, including corpus callosum, with important impact on improving cognition [54]. There are also numerous studies evaluating the effects of CPAP therapy in stroke patients who develop OSA. The stroke can aggravate functional changes and cognition. A study conducted in Korea highlights the beneficial effects of the therapy and suggests that this treatment should be considered as part of the rehabilitation programme for stroke patients. Thereby, CPAP therapy applied to patients with subacute stroke for a relatively short period of time leads to an improvement in sleep quality, daytime sleepiness and cognitive function. Further research regarding the improvement of neurological and functional status among stroke patients, who have received long-term CPAP treatment, is needed [55].
\nIn conclusion, although there are numerous studies that have focused on the association of OSA with cognitive deficits, things are far from fully elucidated. Variate and numerous comorbidities, including ageing, hypoxemia, genetic factors, strokes, etc., independently influence these deficits. Untreated OSA is correlated with changes in brain structure and function through cell death, grey matter destruction, inflammatory changes and decreased white matter integrity. Unlike other pathologies, however, initiating CPAP therapy as early as possible prevents the installation of the cognitive deficiency or improves it if it is already installed.
\nCOPD is a common disease, characterized by persistent respiratory symptoms and airflow limitation caused by significant exposure to noxious particles and gases. COPD is an important cause of morbidity and premature death. According to the WHO, by 2030 it will be the third cause of death worldwide [56].
\nA large meta-analysis which included 23,116 patients with COPD showed an alarming prevalence of MCI, up to 32%, compared with the prevalence of 10–20% in the general population [57]. Furthermore, in time this mild cognitive decline seems to aggravate, and these patients will have an increased risk to develop multi-infarct dementia or Alzheimer’s disease [58].
\nThe origin of the cognitive impairment COPD patients is still not well established. Several pathological relays can interfere: smoking, ageing, severe lung disease, hypoxemia, hypercapnia, systemic inflammation, oxidative stress, endothelial dysfunction, comorbidities, sedentary lifestyle and genetic factors.
\nFrom all the above, hypoxemia seems to be the most important risk factor. Not only continuous hypoxemia but also the intermittent one (during efforts, sleep and daily activities) can cause brain damage [59]. Moreover, a study showed that during COPD exacerbations when hypoxemia worsens, patients have significantly altered cognitive scores compared with those recorded in stable phases and age-matched controls [60]. Neurologic impairment also worsens with COPD progression. In the severe pulmonary disease, altered MMSE scores were reported in 64% of cases [61]. The most common abnormalities in the MMSE included construction (39%), attention (31%), verbal recall (26%), visuospatial orientation (24%) and language (13%). In tasks that required drawing (e.g. an analogue clock with a set time) or other tasks that required judgement, poor performance was associated with a higher mortality [62]. In addition, Chang et al. in a 3-year prospective study showed that the association between COPD and cognitive dysfunction led to increased disability, hospital rate and mortality [63].
\nOne of the most elaborate studies was performed by Dodd et al. [4] who focused on non-hypoxemic COPD patients and combined different brain function assessment techniques such as magnetic resonance diffusion tensor imaging, resting state functional MRI and neuropsychological questionnaires. The report showed that these individuals had decreased integrity of the white matter, dysfunction of grey matter and poor performance in the cognitive questionnaires, compared with age-matched controls. The most significant deficits recorded through imaging techniques were poor executive function, low processing speed and episodic and working memory impairment, which all corresponded with the deficits seen on the MMSE test.
\nThe Rotterdam Study used high-resolution MRI to evaluate cerebral structures in subjects with COPD and reported a higher frequency of cerebral microbleeds. This observation supports the concept of cerebral small-vessel disease that leads to cognitive decline via cerebral micro-bleeding areas. They also increased the MRI performance by introducing voxel-based morphometry analysis. Through this technique, they demonstrated for the first time that even stable COPD patients, who had subclinical cognitive impairment, presented grey matter volume alterations on MRI [64].
\nOther MRI studies revealed a significantly loss of grey matter in numerous brain areas: precuneus, right inferior parietal lobule, right superior temporal gyrus/middle temporal gyrus, hippocampus, limbic and paralimbic structures, cingulate, amygdala, etc. The common aspect in these studies is heterogeneity and broad distribution of the lesions which could explain the multiple and variate neurologic manifestations these patients experience. Moreover, neuroimaging showed that parietal lobule and precuneus are also altered in Alzheimer’s disease.
\nThe psychometric profile impairment correlates with variable components of COPD such as disease severity, exacerbations, hypoxemia or hypercapnia [58]. For accurate results it is indicated to use a battery of tests, not a single one. The most commonly affected cognitive domains are memory, attention, motor and executive function, naming ability and visuospatial orientation [65].
\nOn the other hand, COPD cases without comorbidities are rare. This disease is frequently associated with both respiratory pathologies, like pulmonary hypertension (3–84%), obstructive sleep apnea (58–88%) or lung cancer (3–22%), and non-respiratory comorbidities such as systemic arterial hypertension (14–71%), ischemic heart disease (4–68%), depression (12–49%) and diabetes mellitus type 2 (10–33%) [66]. Although the number of comorbidities rises with age, special caution should be addressed to cognitive-related comorbidities: cerebrovascular diseases, cardiovascular pathology, diabetes mellitus and sleep apnea syndrome. These pathologies should be managed according to current guidelines.
\nStudies show that 50% of COPD patients abandon the prescribed inhaled medication and the oxygen therapy during the first year of therapy and just 25% use oxygen therapy for activities outside their house [67]. Moreover, older COPD patients and those with cognitive impairment have even lower adherence levels to inhalation therapy. The cognitive status impacts patient’s ability to recall when and how to use the inhaler devices. Poor executive functioning is often associated with a “knowing–doing” discrepancy [68]. All these factors listed above have a negative impact on treatment adherence and self-management.
\nThe dyspnea–inactivity–muscular dysfunction circle developed by COPD patients will lead to isolation, depression and low adherence to pulmonary rehabilitation programmes. Given the multifactorial aspects of adherence and the high prevalence of MCI among COPD population, pulmonary rehabilitation programmes should be tailored to subject’s needs.
\nOn the other hand, these programmes have a positive feedback on respiratory symptoms and neurologic function. Therefore, screening for these comorbidities should be considered during baseline pulmonary rehabilitation assessment [69]. Cognitive behavioural therapy or psychological support should be considered when psychological difficulties interfere with disease self-management and adherence [67].
\nAnother condition that should not be ignored in patients with COPD is gait impairment. More evidence suggests that muscle loss, reduced exercise capacity and functional mobility is leading to an important risk of falls. Interventions that include coordination, balance and strength training proved to be effective in older adults [70]. However, balance training and fall prevention strategies are still not mentioned by the pulmonary rehabilitation guidelines, and very few rehabilitation centres have a standardized balance assessment.
\nAlthough regular use of long-term oxygen therapy (LTOT) is correlated with a reduced risk of cognitive impairment in subjects with COPD, it is still under debate when and to whom it should be addressed. However, in patients who develop intermittent hypoxemia (during effort or sleep), earlier oxygen supplementation should be considered in order to prevent irreversible neurologic damage [56].
\nDuring COPD exacerbations in hypercapnic respiratory failure, non-invasive ventilation is a key management tool which markedly reduces mortality and morbidity. Prompt initiation of CPAP therapy prevents the installation of the cognitive impairment [71].
\nPulmonary fibrosis describes the group of fibrosing interstitial lung diseases (ILDs) that causes progressive scarring of the alveolar interstitium, often leading to hypoxemic respiratory failure. ILDs encompass a large and varied group of parenchymal lung disorders, including diseases of unknown cause (idiopathic interstitial pneumonias), as well as those associated with other diseases (connective tissue disease-associated ILDs, chronic sarcoidosis) or environmental exposures (chronic hypersensitivity pneumonitis).
\nIdiopathic pulmonary fibrosis (IPF), the most extensively studied type of ILD, is a relentlessly progressive lung disease with a prognosis that can be worse than many cancers. With a median survival time of 2.5–3.5 years after diagnosis [72], IPF portends substantial morbidity and mortality outcomes, not all of which are directly related to the progressive fibrotic disease itself.
\nThis older population with a median age of 66 years at diagnosis frequently experience various comorbidities, which influence the clinical spectrum, progression and mortality of the disease. An analysis of 272 IPF patients reported that 58% of cases had one, two or three comorbid conditions, 30% had four to seven comorbid conditions and only 12% had no comorbidities [73]. Respiratory comorbidities, including emphysema (8–34%), obstructive sleep apnea (58–88%), lung cancer (3–22%) and pulmonary hypertension (3–84%), were common in many studies, although estimates vary widely depending on the source population. Non-respiratory comorbidities such as gastro-oesophageal reflux (30–80%), systemic arterial hypertension (14–71%), ischaemic heart disease (4–68%), diabetes mellitus type 2 (10–33%) and depression (12–49%) are also highly prevalent [74, 75].
\nRelated to IPF or associated morbidity, there are several potential factors and conditions for the emergence of a cognitive deficit. Hypoxemia, a history of smoking, ageing and chronic evolution of the disease are potential elements for the emergence of a cognitive deficit.
\nDifficulties in breathing (increased intrinsic elastic load of respiratory muscles and stimulation of peripheral mechanoreceptors) [76], night cough, drugs, hypoxemia and obstructive apnea can all alter the quality of life.
\nIPF patients develop progressive ventilatory restriction and exercise intolerance. Alteration of blood gases is a common feature in IPF pathophysiology. Patients experience transient or continuous hypoxia resulting in a substantial cumulative time with an SpO2 below 90%. Nocturnal hypoxia is common in chronic fibrotic interstitial lung diseases, both in patients who associate OSA, as those without this comorbidity. In the absence of OSA, nocturnal hypoxia could be a result of alveolar hypoventilation, altered ventilation-perfusion ratio and a desaturation trend, due to patients on the abrupt portion of the oxygen-haemoglobin dissociation curve [77, 78].
\nEpidemiologic research has shown that besides genetic and environmental factors, such as lifestyles and cardiovascular risk factors, decreased lung function is also associated with dementia and cognitive impairment in the general population.
\nIn a large population-based cohort enrolled in the Atherosclerosis Risk in Communities Study [79], the presence of a restrictive ventilatory pattern was associated with worse performance in cognitive assessments and with an increased risk of dementia hospitalization.
\nA recent prospective study [80] found that patients with restrictive lung disease have almost twice the chance of developing dementia or mild cognitive impairment as healthy individuals. Researchers followed more than 14.000 middle-aged people for over 23 years. Lung disease and impaired lung function were associated with greater risk of dementia and mild cognitive impairment through both Alzheimer’s disease and cerebrovascular aetiologies. Although both COPD and restrictive impairment were associated with increased risk of the dementia phenotypes, magnitudes of association were most pronounced for restrictive impairment. There were no differences between smokers and non-smokers.
\nDifferent pathogenic mechanisms could explain the association of lung function with cognitive performance and risk of dementia. Chronic hypoxia might lead to ischaemic brain injury and neurodegeneration as prospective studies have found that individuals with low lung function or reduced arterial oxygen saturation are more likely to develop white matter lesions and lacunar infarcts [81, 82].
\nA restrictive ventilatory pattern has been associated with the incidence of diabetes and subclinical atherosclerosis and an increased risk of cardiovascular outcomes [83, 84]. In turn, diabetes and cardiovascular disease might cause cognitive impairment and increase the risk of dementia.
\nWorse lung function might cause cognitive impairment and dementia through the development of a pro-inflammatory state. High levels of C-reactive protein, elevated in individuals with reduced lung function, have been associated with a higher risk of dementia [85, 86].
\nIn IPF, a disease with a potential rapid and frequent development of hypoxemia, it is surprising that cognitive impairment has been investigated in very few studies.
\nIn a limited study [87], with only seven IPF patients undergoing pulmonary rehabilitation, applying a battery of five psychometric tests (recall of verbal information, sustained visual attention, efficiency in completing sequential tasks, verbal fluency, visuospatial and graphomotor proficiency) found impaired cognition only on the level of visual attention.
\nA prospective, observational study examining cognitive function in 30 IPF patients with normal oxygen saturations and comparing them to COPD and smoking controls demonstrated that almost half of IPF patients have mild cognitive dysfunction, unexplained by age [88].
\nIn a prospective, cross-sectional, descriptive study [89], Bors et al. showed that individuals with severe IPF have worse cognitive function than those with mild-to-moderate disease and controls. Participants were evaluated through five neuropsychological tests that assessed various domains of cognitive function: speed for attention, sequencing, mental flexibility, visual search and motor function, information processing speed, selective attention, cognitive flexibility, executive function, assessment of verbal recall and recognition and specific cognitive deficits related to accessibility of lexical and semantic information. Severe IPF patients had a significantly inferior performance on tasks requiring speed-divided attention and slower processing speeds when requiring suppression of a familiar response. They are also more likely to have poorer health-related quality of life and symptoms of depression.
\nA cross-sectional study aimed to assess cognition in IPF and to identify clinical cognition modifiers, and 23 IPF patients were evaluated using the Montreal Cognitive Assessment (MoCA) [66]. As it has been previously mentioned, MoCA is a screening instrument with high specificity and sensitivity for detecting early cognitive impairments and is validated in multiple settings and disorders. MoCA evaluates several cognitive domains (short-term memory, visuospatial abilities, executive functioning, attention, concentration and working memory, language, orientation to time and place) to differentiate healthy cognitive ageing from mild cognitive impairment [90]. The study found a mild cognitive impairment in patients with IPF that is related to the areas of visuospatial abilities, language and working memory. Obstructive sleep apnea was highly prevalent in these patients (more than 80% of cases), and there was a significant correlation between cognitive function and the severity of apnea hypopnea index. Poor sleep quality is frequently met in IPF through sleep breathing disorders, including OSA, implying increased sleep fragmentation, decreased slow wave and REM sleep, as well as sleep oxygen desaturation [91].
\nHealth-related quality of life is especially important in this patient population, given the lack of treatment options, poor mortality and rapid progression of the disease. The morbidity associated with IPF has a wide and profound impact on the patient’s quality of life. Therefore, cognition level and other patient-centred outcomes are important goals to be evaluated in clinical research and practice. For IPF we do not currently have a specific cognitive assessment tool, so researchers have used validated tools in cognition analysis of other chronic respiratory diseases. The potential problem is that these tools cannot capture many of the effects of IPF on patients’ lives.
\nPatients with chronic respiratory conditions, such as obstructive sleep apnea, chronic obstructive pulmonary disease or idiopathic pulmonary fibrosis, commonly associate cognitive impairment. Neurologic assessment should be included in the routine diagnostic algorithm of these conditions, in order to appreciate the overall impact of the disease, on patient’s quality of life and prognosis. Physicians who notice signs of memory loss, disorientation, gait impairment or even poor adherence to pharmacologic/nonpharmacologic treatment, should screen their patients for cognitive dysfunction. For a better outcome, subjects who are identified with mild cognitive impairment by a screening tool should be referred for a thorough evaluation to a neurologist, and the chronic lung disease management should be tailored according to individual’s needs.
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