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7 Minute Screen Dementia Pdf 18 [EXCLUSIVE]


The Clock Drawing Test typically requires patients to draw a clock face with numbers and hands indicating a prespecified time. The test was designed as a quick screen for dementia by focusing on the cognitive domains of executive functioning and visuoconstruction.4,24 Based on the Shulman scoring system, a cutoff score of 3 generates the preferred sensitivity (0.86) and specificity (0.96).37 This scale may be used on its own or with other screening tools to assess patients.




7 Minute Screen Dementia Pdf 18



The General Practitioner assessment of Cognition (GPCOG) is a brief dementia screening scale designed for use in primary care.38 It consists of a patient examination and informant interview and takes about 6 minutes. A score of 10 or lower indicates cognitive impairment.


As its name implies, the 7-minute screen takes about 7 minutes to administer and consists of 4 tests that assess memory, verbal frequency, visuospatial skills and visuoconstruction and orientation.39 The test demonstrates a competitive sensitivity and specificity in distinguishing between patients with dementia and normal controls, and its accuracy is not affected by age, sex or educational level.


The Memory Impairment Screen is a 4-item scale designed to detect various types of dementia in different settings.40 The scale has shown good sensitivity and specificity in classifying dementia. A score of 5 or below indicates dementia.


Memantine (Ebixa), an N-methyl-D-aspartate receptor antagonist, inhibits prolonged influx of calcium ions, thereby minimizing neuronal excitotoxicity, a mechanism involved in the neurodegenerative process of AD (Table 4). Memantine is indicated for the treatment of moderate to severe AD.59,60 Memantine is generally well tolerated, and its most common adverse effects include dizziness, drowsiness, constipation, agitation and headaches. Furthermore, a recent meta-analysis of 4 trials showed that combining a cholinesterase inhibitor with memantine in individuals with moderate to severe dementia provided modest benefits in the global clinical impression scale, cognition, behaviour and ability to perform activities of daily living than did monotherapy with a cholinesterase inhibitor.61


Trials evaluating low-dose aspirin, statins, nonsteroidal anti-inflammatory drugs and hormonal replacement therapy showed no benefit on global cognitive and physical function in individuals with MCI or with mild to moderate dementia.62,66


Dautzenberg G, Lijmer J, Beekman A. Diagnostic accuracy of the Montreal Cognitive Assessment (MoCA) for cognitive screening in old age psychiatry: Determining cutoff scores in clinical practice. Avoiding spectrum bias caused by healthy controls. Int J Geriatr Psychiatry. 2020;35(3):261-269. doi:10.1002/gps.5227


There are many causes of cognitive impairment. They include side effects of medicines, blood vessel disorders, depression, and dementia. Dementia is a term used for a severe loss of mental functioning. Alzheimer's disease is the most common type of dementia.


Cognitive testing is often used to screen for mild cognitive impairment (MCI). People with MCI may notice changes in their memory and other mental functions. The changes aren't severe enough to have a major effect on your daily life or usual activities. But MCI can be a risk factor for more serious impairment. If you have MCI, your provider may give you several tests over time to check for a decline in mental function.


Other types of cognitive impairment are not curable. But medicines and healthy lifestyle changes may help slow mental decline in some cases. A diagnosis of dementia may also help patients and their families prepare for future health needs.


If a person has repeatedly taken the test in the same conditions and the total score is the same (25+) but it is taking progressively longer for them to complete each time, exceeding 10 minutes, can this also be indicative of dementia?


Regarding risk stratification approaches, limited evidence was found regarding benefits and harms. Potential benefits of PDMPs and urine drug testing include the ability to identify patients who might be at higher risk for opioid overdose or opioid use disorder, and help determine which patients will benefit from greater caution and increased monitoring or interventions when risk factors are present. For example, one study found that most fatal overdoses could be identified retrospectively on the basis of two pieces of information, multiple prescribers and high total daily opioid dosage, both important risk factors for overdose (124,146) that are available to prescribers in the PDMP (124). However, limited evaluation of PDMPs at the state level has revealed mixed effects on changes in prescribing and mortality outcomes (28). Potential harms of risk stratification include underestimation of risks of opioid therapy when screening tools are not adequately sensitive, as well as potential overestimation of risk, which could lead to inappropriate clinical decisions.


Illicit drugs and alcohol are listed as contributory factors on a substantial proportion of death certificates for opioid-related overdose deaths (contextual evidence review). Previous guidelines have recommended screening or risk assessment tools to identify patients at higher risk for misuse or abuse of opioids. However, the clinical evidence review found that currently available risk-stratification tools (e.g., Opioid Risk Tool, Screener and Opioid Assessment for Patients with Pain Version 1, SOAPP-R, and Brief Risk Interview) show insufficient accuracy for classification of patients as at low or high risk for abuse or misuse (KQ4). Clinicians should always exercise caution when considering or prescribing opioids for any patient with chronic pain outside of active cancer, palliative, and end-of-life care and should not overestimate the ability of these tools to rule out risks from long-term opioid therapy.


Emerging data from early studies -including our own- on postmortem material with the most validated thus far, [F-18]-AV-1451 (T807, Flortaucipir), have shown that this ligand binds with strong affinity to paired helical filament (PHF)-tau aggregates in AD brains and those that form as a function of age [20,21,22, 27, 35], closely matching the stereotypical spatiotemporal progression of neurofibrillary tangles (NFT) as described by Braak [3]. In agreement with these observations, patients clinically diagnosed with dementia of AD type and mild cognitive impairment (MCI) exhibit significantly higher in vivo [F-18]-AV-1451 retention than cognitively normal individuals in regions that are known to contain an elevated burden of tau lesions in AD [4, 6, 7, 11, 16, 25, 28, 33]. The overall utility of this tracer for in vivo selective and reliable detection of tau aggregates in non-AD tauopathies, however, seems very limited with the exception of certain tau mutations causing frontotemporal lobar degeneration (FTLD) characterized by tau aggregates [26] that contain all six isoforms of tau (three-repeat (3R) and four-repeat (4R)) [14] with PHF ultrastructure resembling NFT found in AD. We and others have shown that [F-18]-AV-1451 has low affinity for tau aggregates that contain primarily 4R tau with straight filament ultrastructure that predominate in tauopathies such as progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and most cases of FTLD. We also demonstrated the existence of robust [F-18]-AV-1451 off-target binding to melanin- and neuromelanin-containing cells and some weaker binding to blood components [21, 22]. Controversy exists as to whether AV-1451 may also exhibit significant nonspecific binding to MAO enzymes [12, 15, 17, 30], as it has been recently demonstrated for other tau PET tracers like THK-5351 [13, 24].


To validate the site/s of MK-6240 binding and determine whether there is off-target binding, we examined the regional and substrate-selective autoradiograhic patterns of [F-18]-MK-6240 in postmortem brain, retina and skin tissue samples. Cases with a definite pathological diagnosis of AD, FTLD-tau (PiD, PSP, CBD), chronic traumatic encephalopathy (CTE), FTLD-TDP-43, dementia with Lewy bodies (DLB), cerebral amyloid angiopathy (CAA), metastatic melanoma, brain hemorrhages, and elderly controls free of neurodegenerative diseases were studied. Most of these cases had also been included in our previous validation studies of [F-18]-AV-1451 [21, 22], giving us the opportunity to directly compare the autoradiographic binding patterns of both tracers in comparable tissue samples.


With the purpose of obtaining enough resolution at the cellular level, we dipped adjacent brain slices to those used in phosphor screen autoradiography in a photographic nuclear emulsion. Once the slides are developed, the visualization of silver grains struck by positrons emitted during [F-18] nuclear decay enables precise identification of [F-18]-MK-6240 labeled lesions by optical microscopy.


MK-6240 was identified as a potential imaging agent by screening using cortical homogenates from AD tissue rich in NFT as the binding target and an amyloid plaque tracer for counter-screen [15]. Based on this, we anticipated that MK-6240 would preferentially bind to tau lesions in the form of NFT in AD over other tau aggregates in non-AD tauopathies or lesions primarily made of Aβ, α-synuclein or TDP-43. To date, only very limited data from human in vivo [F-18]-MK-6240 PET imaging studies have been published [2, 19]. Results from these early studies point to a promising 2- to 3-fold higher in vivo [F-18]-MK-6240 retention in neocortical and medial temporal brain regions of AD patients compared to elderly cognitively normal individuals [19]. Because this ligand is already being incorporated into clinical trial research, validation studies such as this paper are absolutely critical to evaluate the potential usefulness of this ligand as a reliable marker of human brain tau lesions. In an attempt to advance towards that goal, we applied [F-18]-MK-6240 phosphor screen and high resolution autoradiography to the study of a series of autopsy samples from individuals with a definitive diagnosis of AD, PiD, PSP, CBD, CTE, CAA, FTLD-TDP-43, DLB, and control brains free of neurodegenerative pathology. Our results confirmed that while [F-18]-MK-6240 avidly bound to PHF-tangle containing slices from AD brains, it did not bind to a significant extent to tau-containing lesions in slices from non-AD tauopathy brains, suggesting that this tracer has higher affinity and selectivity for PHF-tau over tau aggregates with a primarily straight filament ultrastructure, and thus raising reasonable doubts about the potential value of this ligand as a biomarker of tau pathology in non-AD tauopathies. The regional and laminar autoradiographic patterns of distribution of [F-18]-MK-6240, as revealed by the combination of autoradiography using a fine grain nuclear emulsion and immunohistochemistry, closely matched those of classic PHF-tangles in AD brains [1, 18]. Using this method, we confirmed that [F-18]-MK-6240-labeled lesions were NFT, suggesting that these lesions are the main pathological substrate of [F-18]-MK-6240 binding. The microscopic examination of diffuse plaques, CAA, α-synuclein and TDP-43 aggregates confirmed the absence of detectable [F-18]-MK-6240 binding to these lesions, favoring the relative selectivity of [F-18]-MK-6240 for NFT over β-amyloid plaques and other abnormal protein aggregates with a β-pleated sheet conformation.


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