There is a growing population of individuals diagnosed with various forms of Frontotemporal Dementia (FTD) and Primary Progressive Aphasia (PPA), and this number is likely to increase as medical ...practitioners and speech-language pathologists (SLPs) become more expert at identifying these conditions. More clinicians will be seeing, and treating, patients with a diagnosis of FTD or PPA. Toward that end, the goal of this book is to expand this clinical knowledge base and support the development of skills in diagnosis, but also in clinical management.
Dementia is a progressive global cognitive impairment syndrome. In 2010, more than 35 million people worldwide were estimated to be living with dementia. Some people with mild cognitive impairment ...(MCI) will progress to dementia but others remain stable or recover full function. There is great interest in finding good predictors of dementia in people with MCI. The Mini-Mental State Examination (MMSE) is the best-known and the most often used short screening tool for providing an overall measure of cognitive impairment in clinical, research and community settings.
To determine the accuracy of the Mini Mental State Examination for the early detection of dementia in people with mild cognitive impairment SEARCH METHODS: We searched ALOIS (Cochrane Dementia and Cognitive Improvement Specialized Register of diagnostic and intervention studies (inception to May 2014); MEDLINE (OvidSP) (1946 to May 2014); EMBASE (OvidSP) (1980 to May 2014); BIOSIS (Web of Science) (inception to May 2014); Web of Science Core Collection, including the Conference Proceedings Citation Index (ISI Web of Science) (inception to May 2014); PsycINFO (OvidSP) (inception to May 2014), and LILACS (BIREME) (1982 to May 2014). We also searched specialized sources of diagnostic test accuracy studies and reviews, most recently in May 2014: MEDION (Universities of Maastricht and Leuven, www.mediondatabase.nl), DARE (Database of Abstracts of Reviews of Effects, via the Cochrane Library), HTA Database (Health Technology Assessment Database, via the Cochrane Library), and ARIF (University of Birmingham, UK, www.arif.bham.ac.uk). No language or date restrictions were applied to the electronic searches and methodological filters were not used as a method to restrict the search overall so as to maximize sensitivity. We also checked reference lists of relevant studies and reviews, tracked citations in Scopus and Science Citation Index, used searches of known relevant studies in PubMed to track related articles, and contacted research groups conducting work on MMSE for dementia diagnosis to try to locate possibly relevant but unpublished data.
We considered longitudinal studies in which results of the MMSE administered to MCI participants at baseline were obtained and the reference standard was obtained by follow-up over time. We included participants recruited and clinically classified as individuals with MCI under Petersen and revised Petersen criteria, Matthews criteria, or a Clinical Dementia Rating = 0.5. We used acceptable and commonly used reference standards for dementia in general, Alzheimer's dementia, Lewy body dementia, vascular dementia and frontotemporal dementia.
We screened all titles generated by the electronic database searches. Two review authors independently assessed the abstracts of all potentially relevant studies. We assessed the identified full papers for eligibility and extracted data to create two by two tables for dementia in general and other dementias. Two authors independently performed quality assessment using the QUADAS-2 tool. Due to high heterogeneity and scarcity of data, we derived estimates of sensitivity at fixed values of specificity from the model we fitted to produce the summary receiver operating characteristic curve.
In this review, we included 11 heterogeneous studies with a total number of 1569 MCI patients followed for conversion to dementia. Four studies assessed the role of baseline scores of the MMSE in conversion from MCI to all-cause dementia and eight studies assessed this test in conversion from MCI to Alzheimer´s disease dementia. Only one study provided information about the MMSE and conversion from MCI to vascular dementia. For conversion from MCI to dementia in general, the accuracy of baseline MMSE scores ranged from sensitivities of 23% to 76% and specificities from 40% to 94%. In relationship to conversion from MCI to Alzheimer's disease dementia, the accuracy of baseline MMSE scores ranged from sensitivities of 27% to 89% and specificities from 32% to 90%. Only one study provided information about conversion from MCI to vascular dementia, presenting a sensitivity of 36% and a specificity of 80% with an incidence of vascular dementia of 6.2%. Although we had planned to explore possible sources of heterogeneity, this was not undertaken due to the scarcity of studies included in our analysis.
Our review did not find evidence supporting a substantial role of MMSE as a stand-alone single-administration test in the identification of MCI patients who could develop dementia. Clinicians could prefer to request additional and extensive tests to be sure about the management of these patients. An important aspect to assess in future updates is if conversion to dementia from MCI stages could be predicted better by MMSE changes over time instead of single measurements. It is also important to assess if a set of tests, rather than an isolated one, may be more successful in predicting conversion from MCI to dementia.
One of the largest patient populations seen by neuropsychologists are older adults suffering from problems associated with aging. Further, the proportion of the population aged 65 and above is rising ...rapidly. This book provides a guide to neuropsychological clinicians increasingly called upon to assess this population. The book details in a step-by-step fashion the phases and considerations in performing a neuropsychological assessment of an older patient. It covers procedural details including review of patient's medical records, clinical interview, formal testing, interpretation of test scores, addressing referral questions, and preparing an evaluation report.
Key Features* Outlines a clear, logical approach to neuropsychological evaluation* Provides specific clinical practice guidelines for each phase of the evaluation* Integrates clinical practice with up-to-date research findings* Recommends specific tests for evaluating older adults* Details how to interpret test findings and identify the patient's neuropsychological profile* Illustrates important points with examples and case materials, many neuropathologically-confirmed* Includes forms useful in clinical practice
Advances in neuroimaging have enabled greater understanding of the progression of cerebral degenerative processes associated with ageing‐related dementias. Leukoaraiosis or rarefied white matter (WM) ...originally described on computed tomography is one of the most prominent changes which occurs in older age. White matter hyperintensities (WMH) evident on magnetic resonance imaging have become commonplace to describe WM changes in relation to cognitive dysfunction, types of stroke injury, cerebral small vessel disease and neurodegenerative disorders including Alzheimer's disease. Substrates of WM degeneration collectively include myelin loss, axonal abnormalities, arteriolosclerosis and parenchymal changes resulting from lacunar infarcts, microinfarcts, microbleeds and perivascular spacing. WM cells incorporating astrocytes, oligodendrocytes, pericytes and microglia are recognized as key cellular components of the gliovascular unit. They respond to ongoing pathological processes in different ways leading to disruption of the gliovascular unit. The most robust alterations involve oligodendrocyte loss and astrocytic clasmatodendrosis with displacement of the water channel protein, aquaporin 4. These modifications likely precede arteriolosclerosis and capillary degeneration and involve tissue oedema, breach of the blood–brain barrier and induction of a chronic hypoxic state in the deep WM. Several pathophysiological mechanisms are proposed to explain how WM changes commencing with haemodynamic changes within the vascular system impact on cognitive dysfunction. Animal models simulating cerebral hypoperfusion in man have paved the way for several translational opportunities. Various compounds with variable efficacies have been tested to reduce oxidative stress, inflammation and blood–brain barrier damage in the WM. Our review demonstrates that WM degeneration encompasses multiple substrates and therefore more than one pharmacological approach is necessary to preserve axonal function and prevent cognitive impairment.
This article is part of the Special Issue “Vascular Dementia”.
In this review, we discuss disintegration of the cellular components of the gliovascular unit in the white matter. This has consequences on blood–brain barrier integrity and is a strong correlate of white matter damage associated with cognitive impairment. Animal models of cerebral hypoperfusion replicate several features of white matter changes in man. They have been valuable in identifying various agents which target oxidative stress, inflammation and BBB damage.
This article is part of the Special Issue “Vascular Dementia”.
The person in dementia McLean, Athena
The person in dementia,
c2007, 20061001, 2006, 2006-10-01
eBook
"Students of many ilks will benefit from re-imagining Alzheimer's from the perspective of affected elders and their caregivers." - Peter Whitehouse, Case Western Reserve University
•42 trials including 8249 participants are enrolled in our meta-analysis.•A traditional and net meta-analysis was performed to test the diagnostic value of NfL.•NfL increases in all kinds of ...neurodegenerative disease compared to healthy controls.•NfL in CSF and blood differentiates neurodegenerative dementia from healthy controls.•NfL concentration is ranked among neurodegenerative dementia using cluster analysis.
The diagnostic value of neurofilament light chain protein in neurodegenerative dementia diseases is still controversial. A systematic literature search was performed to identify relevant case-control studies conducted through October 2018. Traditional and net meta-analyses were performed based on 42 studies that tested the diagnostic performance of neurofilament light chain protein (NfL) concentration in CSF and serum/plasma from patients with neurodegenerative dementia. CSF and serum/plasma NfL levels were significantly increased in patients with neurodegenerative dementia diseases. Network meta-analysis showed a significant reduction in CSF NfL levels during mild cognitive impairment, whereas an increase was observed in vascular dementia compared to Alzheimer’s disease. Surface under the cumulative ranking curve and cluster analysis showed that the NfL concentration in CSF (vascular dementia, frontotemporal dementia, and Alzheimer’s disease) and serum/plasma (frontotemporal dementia and Alzheimer’s disease) ranked first among neurodegenerative dementia diseases. NfL is an important biomarker that can help clinical neurologists make early diagnoses of neurodegenerative diseases, so patients can receive prompt treatment.
Poststroke cognitive impairment and dementia (PSCID) is a major source of morbidity and mortality after stroke worldwide. PSCID occurs as a consequence of ischemic stroke, intracerebral hemorrhage, ...or subarachnoid hemorrhage. Cognitive impairment and dementia manifesting after a clinical stroke is categorized as vascular even in people with comorbid neurodegenerative pathology, which is common in elderly individuals and can contribute to the clinical expression of PSCID. Manifestations of cerebral small vessel disease, such as covert brain infarcts, white matter lesions, microbleeds, and cortical microinfarcts, are also common in patients with stroke and likewise contribute to cognitive outcomes. Although studies of PSCID historically varied in the approach to timing and methods of diagnosis, most of them demonstrate that older age, lower educational status, socioeconomic disparities, premorbid cognitive or functional decline, life-course exposure to vascular risk factors, and a history of prior stroke increase risk of PSCID. Stroke characteristics, in particular stroke severity, lesion volume, lesion location, multiplicity and recurrence, also influence PSCID risk. Understanding the complex interaction between an acute stroke event and preexisting brain pathology remains a priority and will be critical for developing strategies for personalized prediction, prevention, targeted interventions, and rehabilitation. Current challenges in the field relate to a lack of harmonization of definition and classification of PSCID, timing of diagnosis, approaches to neurocognitive assessment, and duration of follow-up after stroke. However, evolving knowledge on pathophysiology, neuroimaging, and biomarkers offers potential for clinical applications and may inform clinical trials. Preventing stroke and PSCID remains a cornerstone of any strategy to achieve optimal brain health. We summarize recent developments in the field and discuss future directions closing with a call for action to systematically include cognitive outcome assessment into any clinical studies of poststroke outcome.
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