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I have been having some difficulty in understanding the OASIS-3 (Open Access Series of Imaging Studies) database for neuroimaging datasets for cognitively normal and cognitively declining patients (e.g., Alzheimer's disease). There are several respondents who received a "Cognitively Normal" remark for the first diagnosis, while having various remarks for the second diagnosis, particularly: Active/Remote Mood Disorder, Remote Hypothyroidism, Active Bereavement, and Active Alcoholism. Can these "disorders" or "impairments" be classified under Mild Cognitive Impairment (MCI) to eventually lead to Alzheimer's disease or other decline/change in cognitive performance?
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MCI has two types, amnestic and nonamnestic (first ref above). The diagnostic criteria and guidelines are available (second ref). There are other resources you could explore. Good luck.
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I am trying to see how can I identify those patients who have converted to AD from MCI within a certain period, in the ADNI database without having to go through each and every scan in the database.
I know that there are some meta-data given through CSV files on the scan, in the ADNI website but I did not manage to identify a pattern which can help me achieve my goal.
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might be useful, MC
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I want to classify the early-onset alzheimer's and for that i need a database that contains Mild Cognitive Impairment (MCI), Subject Cognitive Impairment (SCI), Alzheimer's disease (AD) and Health controls (HC).
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Appreciating your wish for a compact dataset - if you do not include a detailed social and medical history you'll miss the opportunity to detect false positives. Spouses and others close to the client will have observations that can prove that positive signs have the long history required for a diagnosis of SDAT. Medical history will rule out the many other possible causes for early cognitive decline.
Good fortune on your work, Psychologist Paul McGaffey, PhD(ABD)
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am working on machine learning for early prevention technique
for mild cognitive impairment symptoms
that prevent dementia
and I need DataSet resources
any suggestions/recommendations ?
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You can request access to public datasets from different cohorts at http://www.gaain.org/
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Difference between SCC and SCD/SCI
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I agree with what Jordi said. I would add to it that it can be very helpful to differentiate between subjective cognitive impairment and subjective cognitive decline. A different 2014 paper by Frank Jessen argues for using the term subjective cognitive decline in research on aging/neurodegenerative disorders, given the progressive nature of these diseases. I've found this paper really helpful in conceptualizing these ideas.
Jessen, F., Amariglio, R. E., Van Boxtel, M., Breteler, M., Ceccaldi, M., Chételat, G., ... & Glodzik, L. (2014). A conceptual framework for research on subjective cognitive decline in preclinical Alzheimer's disease. Alzheimer's & Dementia, 10(6), 844-852.
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depression can be a prodrome or a comorbidity of lewy body disease or other cognitive issues (alzheimer, mci, ...)
In which case the psychiatrist must investigate for the lewy body disease ? 
With which tools ?
Kinds regards 
RaphaËl
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as regarding tools: for visuospatial dysfunction seen in DLB Mini Mental State Examination (MMSE) is not a great tool and other tests like clock drawing may be better.
For REM sleep behaviour disorders apart from history, polysomnography is required for confirmation.
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I am interested in the topic of mild cognitive impairment and how early diagnosis will help prevent progression to Alzheimer's disease or dementia. Can someone suggest an intervention or tool that could measure MCI and maintain or improve functional independence respectively? Thank you.
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Kathryn, Your good question raises complex questions. My practise for the last 35 years has included a large focus on diagnosis of early dementia. Along the way, such referrals started using the phrase "MCI", instead of querying early dementia. Thus, for doing research, you'll want to  define MCI in a way that distinguishes it from early dementia; I have been unable to do so. Instead what I found fit the MCI referrals into a false-positive space. For a few examples: people who were chronically depressed or were chronic Marijuana users and whose attentional initiative was inactive (executive disuse), or those who were experiencing chronic thyroid dysfunction. All of these could of course be treated once identified.
Another way of advising you is to suggest that there are no norms for MCI, and that this may be due to careless definition of the term. So if you believe in the concept of MCI, it is incumbent on you to prove the concept, rather that assuming it to be real. Such a study would have utility.
Looking forward,     Psychologist Paul McGaffey
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There are many different terms for SCI, thus I also refer to subjective memory impairment (SMI), subjective cognitive complaints (SCC) etc... and subjective cognitive decline (SCD) which is the more appropriate term when referring to the decline associated with further cognitive impairment (i.e. to MCI or AD).
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We are currently working on this topic, but I have not examined the data as of yet.
We recently published a paper on objective versus subjective cognitive functioning in persons with and without chronic stress. You can find it on this site. We did 24 hour urinary cort over two years as well as cog measures three times over that period. I hope you stay in touch. 
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Hi, I need a computer program that can do a baseline and then a retest after a 4 week intervention for patients with MCI, and preferably the same program should be able to test patients with negative symptoms/cognitive symptoms of schizophrenia. Thanks
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We would like to use the FCSRT in our clinical routine but we don't find any standardized norms for the German version. Could maybe someone, who is using the FCSRT not only for Research, tell me where I could find reliable norms or which cut-offs they use?
Thank you!
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Hi Lara,
thank you very much for all the Information! It is very helpful!
Regards,
Sarah
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I'm conducting quali research with women with Turner Syndrome, which is associated with a particular cognitive profile. I'm pretty sure how I'm going to adapt the interview methodology around this but would like to find out what other people have done. 
Anything where researchers show how they've adapted methods to be more accessible would be of interest.
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Will. thanks for your thought-provoking and helpful comment and the references.
It is interesting, the presumption that people who have a disability of some kind are automatically vulnerable, particularly as in ethics guidelines it often isn’t explained what it is about having a disability might make someone vulnerable. Does it depend on the type of disability? How does that interact with the individual’s own situation: ie their experience of having that disability or the way they manage it could vary? It is interesting to think about.
Liz, yes, I am planning for my screening questionnaire to include questions about adaptions. Although I’m a bit concerned that giving participants too many options might present problems for people with executive function difficulties, who find it hard to make decisions, so it would be good if I could take on some of that myself where possible. Some of this will get untangled by piloting it.
This is a PhD project but I’m a mature student; I’ve volunteered in the fertility field for a while and have conducted related research before. I also used to be an accessibility tester/auditor and, while I haven’t worked directly with people with disabilities very often, I understand how adaptions can be put in place. It’s more about which ones to use and in which circumstances.
 I’ve also spoken to the TS charity and a couple of TS doctors and got the impression that I was being overly cautious in going to lengths to make my research methods accessible. If the participant group and the charity that represents them doesn’t consider themselves to have a disability then who am I, etc etc. However on the other side, there is the research evidence. My participants will be women who are looking at egg donation or adoption as a method of family-building (and most will have partners) so (from my perspective) the issue is not one of capacity, it’s about creating an environment where they feel able to say what they want to say in the way that works best for them and causes the least possible stress. Hence I’m tweaking a standard method rather than going for a participative approach.
I hadn’t heard of Kirsty Liddiard so thanks for that tip.
And Paul, thank you for your thoughtful comment.
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MCI= Mild Cognitive Impairment
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Thank you for your opinion.
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I am aware of a University of Georgia doctoral candidate who is studying this test as a means of detecting early onset dementias.  This test has also been used to indicate fatigue in sleep research.  I am interested in this test as a simple and fundamental way of using sensory perception variability to track episodic mild cognitive impairment over time (as a clinical tool in primary care).
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Dessyedee. Critical Flicker Fusion was used a lot in medicines research in the 80's and 90's. It's main advocate was Ian Hindmarch at the University of Leeds and more recently Keith Wesnes in his battery of computerised cognitive tests.  I suggest you Google their names and you should get a lot of references. I am fairly sure that Keith has developed it for clinical use.  It is very sensitive, even to levels of arousal in the circadian rhythm.  Good hunting.  Andrew.
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The Rapid Cognitive Screen(RCS): A quick screen for Mild Cognitive Impairment
An in depth validation of the RCS has recently been validated. This test takes two and a half minutes to complete. It is superior to the Minimental status(MMSE)  and the MiniCog at identifying persons with early cognitive dysfunction. It is derived from the well validated St Louis University Mental Status (SLUMS) examination. It is available in 25 languages  http://aging.slu.edu/index.php?page=multi-language-slums.
This is an ideal screener for general practitioners and primary care practitioners. 
The Rapid Cognitive Screen (RCS): A Point-of-Care Screening for Dementia and Mild Cognitive Impairment. - PubMed - NCBI
J Nutr Health Aging.The Rapid Cognitive Screen (RCS): A Point-of-Care Screening for Dementia and Mild Cognitive Impairment.
Malmstrom TK Voss VB Cruz-Oliver DM Cummings-Vaughn LA Tumosa NGrossberg GT Morley JEAuthor information
1Theodore K. Malmstrom, PhD, Department of Neurology and Psychiatry, School of Medicine, Saint Louis University, 1438 South Grand Boulevard, St. Louis, Missouri 63104,
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John,
Agree that older adults should be examined for cognitive impairments. But, we should also draw a line, somewhere. Blood tests are not done for all patients visiting health professionals! Why shouldn't we follow that example for cognition? Not sure, if time/cost efficiency justifies doing screening tests, either. When looking at the staggering number of wrongly diagnosed AD patients (some say >45%), I really become suspicious of screening measures efficacy (even though as a board certified clin psych, I should be defending these measures).
But, performing better than MMSE, is promising for RCS. I was wondering if the RCS has been examined against MOCA? Thanks.
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I'm looking broadly into the possibility to offer cognitive training to our patients with MCI. What are your experiences? I am interested in which types of training has been tested, the outcome and what the patients themselves have thought about it. Thank you for any comments!
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It's an exciting and growing field. Above comments make sense.
Last year I submitted my thesis at the university of Oslo and Dalhousie University. Although our target population was people with cochlear implants and hearing aids, you may still find my thesis useful. 
All the best,
Amit
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There is a consensus among researchers that late life depression and depression in AD comprehend two different pathologies, with some shared symptoms. For example, apathy and amnesia are common features in both diseases, and could be explained by consequences of a mood disorder or a cognitive syndrome. In addition, frontal lobe dysfunction is linked to a variety of geriatric neuropsychiatric syndromes, representing an area of intersection in depression and dementia (Steffens, 2012).
Therefore, identification of depression as marker for increased risk of conversion from depression to dementia among patients with MCI has become the main focus for those caring for individuals with depression or cognitive impairment. We now need further investigation. 
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I agree, further investigation is needed in this area. I recently saw a patient who had been evaluated at two other occations. At each neuropsychological evaluation she endorsed clinically significant depression, but otherwise her profile was normal. At her most recent evaluation, she remained depressed, but now had significant memory impairment. Although her ADLs were still intact, it is easy to speculate that she might eventually meet criteria for dementia.
The more we know about depression and how it relates to cognitive impairment, the more we will be able to do for our patients. Thank you for posting this!
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Neuropsychiatric symptoms (NPS) in dementia have been described since Alois Alzheimer’s index case of Auguste D, who presented initially with emotional distress and delusions of infidelity. NPS are common in dementia with prevalence rates of up to 97%. Over time, NPS have become understood to becore symptoms of dementiaand are included in the most recent criteria for all cause dementia. NPS in dementia are associated with faster cognitive decline and acceleratedprogression to severe dementia or death, higher rates of institutionalization, greater functional impairment, greater caregiver stress, worse quality of life and higher burden of neuropathological markers of dementia. NPS are also present in Mild Cognitive Impairment (MCI) with a prevalence of 17-55% and are also associated with poorer outcomes, increased neuropathological burden and faster conversion to dementia, compared to patients without NPS. Evidence now suggests that NPSin the absence of cognitive symptoms may manifest as the initial symptoms of neurodegenerative disease. 28% of dementia cases are initially given psychiatric diagnoses and they present with psychiatric symptoms such as apathy, anxiety, depression or mania. However, there is no systematic method of diagnosing these early NPS and much further work in this area is required.
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The symptom are quite common and epidemiological studies support a conversion rate between 15% to 30 %.  Review the following papers by Morris and Petersen:
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See above
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The most used currently may be the MOCA test, Montreal Cognitive Assessment test.  It is online at MOCAtest.org, Here is a link to a citation for the german translation: https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0032-1301641
Hope this is helpful.  MMSE is now a copyrighted test and you need a license to use it or you could pay a fine. 
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It is well established that patients with Parkinson's disease show impairments in various cognitive processes including executive function when assessed using computerised cognitive tasks such as the CANTAB battery. A number of pharmaceutical companies are developing drugs for the treatment of cognitive dysfunction in Parkinson's disease including Parkinson's disease MCI.
However, when one looks at research investigating "the patient prospective", cognitive dysfunction is not among the most troubling symptoms reported by patients with early or mid-stage Parkinson's disease.
I have two questions.
1. Do clinicians believe that cognitive dysfunction in early or mid-stage Parkinson's disease affects their day to day functioning (i.e. activities of daily living) and do patients worry about their cognition?
2. Do you think Pharmaceutical companies should keep investing in the development of novel compounds for cognitive enhancement in Parkinson's disease?
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Thank you all, for your thoughtful comments.
1. I think while there is no doubt that there are significant cognitive deficits in PD and this may in part be made worse by other non-motor symptoms like depression, anxiety, sleep disturbances etc. I still think there is very little work done to show how this impacts on functional outcome such as activities of daily living. We need to do more research in this area.
This is important for those of us involved in drug discovery because the FDA and other regulatory authorities want us to demonstrate an effect of the drug not only on cognition as measured by various cognitive tasks, but also some measure of functional outcome. They will not approve a drug for cognition unless there is a change in activities of daily living.
2. I agree with the comments made about PD being a heterogeneous disorder. I think one would need to define the sub-group of patients that would most benefit from the drug by focussing on a specific phenotype that is common regardless of the underlying mechanism. For example, one could focus on the PD-MCI group with executive deficits and for this group one would aim to develop drugs that increase cortical dopamine.
While cholinesterase inhibitors such as Rivastigmine is approved for PD-dementia, the efficacy is rather modest and there is still an unmet need for drugs with substantially greater efficacy.
3. I agree that the way forward is to develop disease modifying drugs that target the underlying pathology (for example, an antibody for alpha-synuclein), but I think there is still room for symptomatic treatments and one could potentially achieve greater improvements in cognition with a combined treatment approach. Furthermore, I agree that we should think about non-pharmacological approaches that might work synergistically with pharmacological treatments for cognition (i.e. cognitive training + drugs that enhance synaptic plasciity).
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The standard tests used in memory clinics e.g. The Montreal Cognitive Assessment (MoCA); Mini Mental State Examination (MMSE); Addenbrooke’s Cognitive Examination (ACE-R); The Trail Making Test etc… are not sensitive enough to pick up very early signs of cognitive impairment. I am currently reviewing the SCI literature for my PhD but I have not yet come across any sensitive enough measures. Is anyone aware of any being developed?
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Regarding some current research on cognitive measures for "early detection", see the following recent review article:
Dorene M Rentz , Mario A Parra Rodriguez , Rebecca Amariglio , Yaakov Stern , Reisa Sperling and Steven Ferris. Promising developments in neuropsychological approaches for the detection of preclinical Alzheimer’s disease: a selective review.
Alzheimer's Research & Therapy 2013, 5:58 (21 November 2013)
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I am looking for information regarding what different memory clinics do when they are presented with someone showing signs of subjective cognitive impairment (SCI). Specifically I am looking at people who present at a memory clinic complaining of a problem with their memory but no paper-based measures pick it up. These people will not have any objective cognitive impairment but know that something is not right. All clinics will look at possible alternative explanations for the SCI e.g. depression, but what I am interested in is what happens to that person when they cannot identify an alternative explanation. Some clinics operate an ‘open door policy’, thus they can contact the clinic for an appointment if they feel their impairment has worsened. Other clinics will discharge them from the service, and if their impairment worsens then they have to go back to their GP and be re-referred to the clinic. I welcome any additional thoughts or suggestions on this area.
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Dear Amy,
Approximately one third of the population of our Dementia Service Centers are in the early stages of dementia (Auer et al, 2013). Persons with SCI are worried about their cognitive abilities and we should not send them away with an uncomfortable feeling- or worse telling them that everything is alright (even though they feel differently). We have developed a prevention training program that we offer to persons who would like to do something against their subjectively perceived loss of cognitive functions. In general a health psychological approach is suggested in which a healthy life style is promoted and persons get support to reach their new personal goals. Programs need to be developed and tested for efficacy
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Cognitive impairment is an under-recognized component in HF. Not only do clinicians fail to recognize it but it may have a substantial impact on the ability of patients to perform self-care and stay out of the hospital?
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Many clinical studies have focused on the evaluation of screening tools to assess cognitive impairment in patients with heart failure (HF), yet there's no consensus on standard or specific set of tests or questionnaires to be applied. The pattern of cognitive deficits among people with HF, is similar to those found among patients with vascular cerebral impairment (i.e. attention, psychomotor speed, and executive impairment in particular, memory impairment).
Davis K and Allen J, in a review of litterature (Heart Lung 2013) published from 2000 to 2011 (23 studies) identified 7 screening instruments amongst which the Montreal Cognitive Assessment (MoCA) appeared to be a suitable screening tool in this population.
A paper from Cameron J et al. (European journal of Heart Failure, dec 2013) is newly published on this topic too.
Best regards
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Provisional research diagnostic criteria for Mild Behavioral Impairment (MBI)
A. Behavioral concern reflecting a change in behavior observed by patient or informant or clinician, starting later in life (age≥50) and persisting at least intermittently for > 3 months. These represent clear change from the person’s usual behavior as evidenced by at least one of the following:
a. Decreased motivation (e.g. apathy, aspontaneity, indifference)
b. Affective lability (e.g. anxiety, dysphoria, changeability, euphoria, irritability)
c. Impulse dyscontrol (e.g. agitation, disinhibition, gambling, obsessiveness, behavioral perseveration, stimulus bound)
d. Social inappropriateness (e.g. lack of empathy, loss of insight, loss of social graces or tact)
e. Abnormal perception or thought content (e.g. delusions, hallucinations)
B. Behaviors are of sufficient severity to produce disability in at least one of the following areas:
a. Interpersonal relationships
b. Other aspects of social functioning
c. Ability to perform in the workplace
C. While co-morbid conditions may be present, the behavioral changes are not attributable to another psychiatric disorder, or vascular, traumatic or medical causes, or the physiological effects of a substance or medication.
D. The patient does not meet criteria for a dementia syndrome (e.g., Alzheimer’s dementia, frontotemporal dementia, dementia with Lewy bodies, vascular dementia, other dementia). Mild Cognitive Impairment can be concurrently diagnosed with Mild Behavioral Impairment.
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After reading your question globally, I would say that if we take into consideration all of what you bring into the question, I would add another concept. The concept in the elder population is a murky hopelessness and realization of the end of the "possibles" in life, leading to generalized reconditioning. More of the constructs and articulation of the phenomenon need to be explored as a concept.
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In many publications, researchers compare measures using a screening procedure between extreme conditions of interests (those highly affected vs. healthy) without including patients for which the test is most likely to be used on; those for which the situation is not clear.
In your analysis, you compare AD patients to healthy patients without including those with MCI. However, in practice, we are likely to use the instrument on patients with the entire spectrum of severity of dementia. Your results are therefore only valid if we can previously exclude those with MCI and then use the test.
How is this clinically feasible?
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Thanks for your interest and your comments. I attach supplementary data with 2 options
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Patient is a native German, Polish as a second language in her mid-twenties, still using both Polish and German, now presenting problems with discourse, fluency and naming in both languages. Memory and executive functions persevered, mild attentional deficits.
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Anna, I'm inclined to agree with Stephen that PPA looks most likely at present.
Given she's functioning well I would 'watch and wait'. This early, scanning probably won't add much, but would give you a baseline to compare to in a year or two.
A study in 'Brain' a few years back found 20-33% of focal and language based dementias showed Alzheimer's pathology at autopsy and this was a little more often the case in those >80, so although she doesn't look like a typical Alzheimer's person, that may still be the case. Whether cholinesterases work in that subgroup I don't know, I would guess not.
Hope this helps, I would be interested to hear the final outcome,
Jonathan
P.s. I'm no great expert either!
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I am looking for some hands-on activities that could be utilized to educate a child with mild down syndrome, a moderate hearing defect and speech disorder.
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I do not share some concepts you use in the question: we educate pupils or persons, not patient; and I never understand why we talk about activities for Down syndrome children, because they do not need different activities. Everyone needs the activities that connect news learnings with the zone of proximal development. This kind of thoughts (based in social model of disability in the place of medical model) lets new emergent realities: people with Down syndrome can break away to find new ways. Here you are an example.
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I found in a case-control study that they smoke and drink much more. This is another interesting article: I think we have to pay attention to this because ADHD has a huge prevalence (3 to 6% in children and 50% of persistence in adults): Ivanchak, N., Fletcher, K., & Jicha, G. a. (2012, October). Attention-deficit/hyperactivity disorder in older adults: prevalence and possible connections to mild cognitive impairment. Current psychiatry reports. doi:10.1007/s11920-012-0305-8
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Hi Andre'
This is a very interesting question. As a developmental paediatrician I have often wondered about long-term implications for children with ADHD apart from those known in psychosocial and psychaitry literature. One could postulate that since frontal lobes and deeper striatal pathways are involved in ADHD maybe this could link to increased risk for dementia? However, I do not know of any specific studies done to examine this question.
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The so-called depressive pseudodementia, also known as depression-related cognitive impairment, dementia syndrome of depression, depressive dementia, is controversial in its origin, its alleged reversibility and its epidemiology. It is well known that cognitive disturbances, especially regarding attention, memory and executive functions can be present in depressed patients, completely or partially reversible after antidepressant therapy, and cases of reversible MCI with depressive symptoms are reported in literature. However, a symptomatology that simulates a dementia condition due to depression or other psychiatric disorders seems quite rare if not exceptional. Is pseudodementia a realty or hope?
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Pseudodementia is a commonly referred to "diagnosis," but is it real? I think one of the reasons it has been perpetuated as a diagnosis is that it is intriguing to discuss and fun to use as a teaching point for our residents and students, much like the apathetic presentation of hyperthyroidism in certain geriatric patients - it's a great trick question on rounds and in quizzes / tests, etc.
I believe it is a real entity, but it is likely not depression masquerading as dementia so much as an early manifestation of dementia. This is the observation noted in the earlier entry by Lisa Catapano-Friedman, that it is often atypical and is usually a first in life-time change, which should raise a red flag, as first onset depression in late life not due to situational factors is relatively uncommon.
A foundational underpinning in the literature which finally gave some clarity on this is the autopsy study by B.C. Jost and George T. Grossberg in the Journal of the American Geriatric Society, 1996, vol 44, pp 1078-81. It was a large (for an autopsy study) Alzheimer's study looking retrospectively at time and incidence of behaviors in a population with 100% advanced Alzheimer's the time of death. They assessed several major factors: 1) the average length of time prior to death that each dementia-related behavior emerged, 2) the percentage of patients having those symptoms, and 3) the average length of time the diagnosis of dementia was made prior to death (approximately 30 months).
Of 16 behavioral symptoms / diagnoses evaluated, depression was the third most common (at slightly over 50% of patients) and the third earliest (peak incidence at about 53 months prior to death). This means the peak incidence was approximately 2 years prior to the diagnosis of dementia itself, which goes very much along with the "depression is an early symptom of dementia" theory, which is not longer a theory in light of this and other studies. Though a few of these study patients with depression may be rare late life onset cases, the majority are obviously early manifestations of dementia, thus literally proving that patients were diagnosed with depression and that it was not recognized for what it was (early dementia).
Some of the extremely powerful elements of this study are the fact that all cases are autopsy-confirmed Alzheimer's and that all patients selected had no history of any psychiatric diagnoses or behaviors earlier in life, so this becomes a cornerstone reference for this disease as it relates to its associated behaviors.
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Mild cognitive impairment (MCI) diagnosis is generally accepted as an intermediate condition between cognitive non-normality and dementia. Nevertheless, the exact role of cognitive and daily living autonomy assessment remains quite indefinite. For example, ADL and IADL and MMSE must be normal? The concept of 1.5 standard deviation different from the cognitive performance of a standardized sample, is not very clear neither completely reliable. The use of equivalent points is not diffuse in all countries. Standardized neuropsychological tests are not always available as well as standardized translation of tests. A minimal but sufficient battery of neuropsychological tests has not yet been defined nor widely accepted. For these reasons, MCI diagnosis criteria can be quite different in the some studies, determining differences in findings of epidemiology and in conversion rate from MCI to dementia. What are the proposals to overcome these issues?
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It is a great how hard question. For instance, we are working to developing a basic test for the evaluation of the memory / cognition of the space (Caffò et al. 2012 AJAAD, DOI: 10.1177/1533317512452035). We considered Petersen's criteria too strict at least for the people we work with, often with a very low level of education. For the definition of aMCI we established that at least two memory tests should be impaired. For the diagnosis of naMCI was necessary that at least two neuropsychological, not memory, tests showed to be impaired (usually those pertaining the area of ​​executive functions). For the diagnosis of multiple domains we set a criterion of four tests impaired. Obviously, any strategy seems to be too little or too severe. We had the feeling that even when patients failed to neuropsychological tests, their performance in daily activities wasn't so compromised. We also became convinced that major markers are those that indicate a change in habits: "I ​​do not drive anymore because I get lost in the streets", "I do not play more cards because I forget my previous hands." In other words, I believe that a well-motivated group of researchers could build a test/interview able to capture the change in daily life, before the deterioration is blown.