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I'm a fan of Psychology.
I'd like to know what "pseudo debility" is. Unfortunately, I don't know what it means in English. This is my free translation from Russian.
I've encountered the terms "pseudo debility" and "digital dementia" on resources that popularize science. But I still haven't found a generally accepted definition.
This "pseudo debility" is the simplification and flattening of delirium in the modern world. In the past, delirium was more saturated, unique and striking imagination.
I'd like to know:
- What is it?
- Who invented and studied it?
- Цифровое слабоумие: кто на самом деле глупеет от гаджетов?
- Псевдодебильность и слабоумие общества. Андрей Курпатов на QWERTY
The video above refers to such authors as Manfred Spitzer and Theo Compernolle
Digitale Demenz is a book by Manfred Spitzer
"Digital dementia" seems to be (from de.wiki link) an idiosyncratic (and pejorative) term used to describe a high dependence on portable electronics like smartphones, notebooks. See e.g.
"Why Smartphone Dependence Is Ravaging a Generation" obviously from an alarmist proponent of this phenomenon, or "Mobile phone overuse" on Wikipedia for a more neutral perspective.
the more general term seems to be "overuse of technology". Calling it "dementia" probably relates to an influential article (discussed in the previous link) titled "Is Google Making us Stupid?". Another pejorative term is "digital zombie".
From the absence of sources you provided, I don't know what "pseudo debility" might be, but based on your def "simplification and flattening of delirium in the modern world" it doesn't sound terribly related to "digital dementia" in the sense used by Manfred Spitzer.
Digital pseudo debility is used by a popular Russian psychiatrist Andrey Kyrpatov to describe a dependence, addiction to information on smart phones, ipads, etc. people think they are getting smarter when in reality they exhibit all signs of dependence . He also describes in medical terms what exactly happens in a brain of an addicted person. So digital dementia is the closest to digital pseudo dibility. https://snob.ru/selected/entry/99993 Translated excerpt from the article : “ Only one thing differs from clinical debility and pseudo-debility: there is no way to make/force, under any circumstances, a clinical moron to think; the state of his grey matter won't allow that. But the "gray matter" of information psevdodebil is safe, and, in principle, his brain can be trained. But why? No, why not to train him, and why should he train it? What's the point? What is the motivation? Will he somehow be respected for this in a special way? Or, on the contrary, will they shame that he is a fool? Or he will not survive without it? Not.”
What is pseudo debility? By Andrey Kurpatov https://www.erarta.com/ru/museum/news/report/detail/news-02928/
Kill the idiot inside you. Information pseudo-debility and digital dementia.https://cont.ws/@adviser095/913341
Baizerman, M., & Ellison, D. L. A social role analysis of senility.Gerontologist, 1971,11, 163–170.
Bergmann, K., Foster, D., & Kay, D. W. K. The need for an integrated geriatric service. InPsychiatric disorders in the aged. Symposium presented at the meeting of the World Psychiatric Association, Royal College of Physicians, London, September 28–30, 1965.
Bollerup, T. R. Prevalence of mental illness among 70-year-olds domiciled in nine Copenhagen suburbs.Acta Psychiatrica Scandinavia 1975,51, 327–329.
Brocklehurst, J. C. Brain failure in old age—Social implications.Age and Ageing, 1977,b(Supplement), 30–41.
Butler, R. N., & Lewis, M. I.Aging and mental health: Positive psychosocial approaches. St. Louis: C. V. Mosby, 1973.
Butler, R. N.Why survive: being old in America. New York: Harper and Row, 1975.
Clemmey, R., Kennard, D., & Mandelbrote, B. The assessment of social breakdown in newly-admitted psychiatric patients.British Journal of Psychiatry 1975,127, 417–431.
Ellsworth, R. Consumer feedback in measuring effectiveness of mental health programs. In M. Guttentag & E. L. Struening (Eds.)Handbook of evaluation research. Beverly Hills, California: Sage Publications, 1975.
Godber, C. Planning services for the elderly demented patient.Age and Ageing, 1977,b Supplement, 100–103.
Grad de Alarcon, J. Social causes and social consequences of mental illness in old age. In D. W. K. Kay & A. Walk, (Eds.),Recent developments in psychogeriatrics: A symposium. Ashford, Kent: Royal Medico-Psychological Association, 1971.
Gruenberg, E. M. Community conditions and psychoses of the elderly.American Journal of Psychiatry, 1954,110, 888–896.
Gruenberg, E. M. A mental health survery of older persons. In P. H. Hoch & J. Zubin (Eds.),Comparative epidemiology of mental disorders. New York: Gruen and Stratton, 1961.
Gruenberg, E. M. The social breakdown syndrome—Some origins.American Journal of Psychiatry, 1967,123, 1481–1489.
Hoening, J. & Hamilton, M. W.The desegregation of the mentally ill. London: Routledge & Kegan Paul, 1969.
Kay, D. W. K., Bergmann, K., Foster, E. M., McKechnie, A. A., & Roth, M. Mental illness and hospital usage in the elderly: A random sample followed up.Comprehensive Psychiatry, 1970,11, 26–35.
Kay, D. W. K., & Walk, A. (Eds.).Recent developments in psychogeriatrics: A symposium. Ashford, Kent: Royal Medico-Psychological Association, 1971.
Kobrynski, B. The mentally impaired elderly—Whose responsibility?Gerontologist, 1975,15, 407–411.
Krause, A. S., Spasoff, R. A., Beattie, E. J., Holden, E. W., Lawson, J. S., Rodenburg, M., & Woodcock, G. M. Elderly applicants to long-term care institutions. I: Their characteristics, health problems, and state of mind.Journal of the American Geriatrics Society, 1976,24, 117–125.
Kreisman, D., & Joy, V. The family as reactor to the mental illness of a relative. In M. Guttentag and E. Struening (Eds.)Handbook of evaluation research. Beverly Hills, California: Sage Publications, 1975.
Kuypers, J. A., & Bengston, V. L. Social breakdown and competence: A model of normal aging.Human Development, 1973,16, 181–201.
Lasswell, T., Burma, J., & Aaronson, S. (Eds.),Life in society: Introductory readings in sociology. Chicago: Scott, Forseman, 1965.
Lezak, M. D. Living with the characterologically altered brain injured patient.Journal of Clinical Psychology, 1978,39, 592–598.
Libow, L. S. Pseudo-senility: Acute and reversible organic brain syndromes.Journal of American Geriatrics Society, 1973,21, 112–120.
Lowenthal, M. F., Berkman, P. L., and Associates,Aging and mental disorder in San Francisco, San, Francisco: Jossey-Bass, 1967.
Macmillan, D. Features of senile breakdown.Geriatrics, 1969,24, 109–118.
Maddox, G. L. The patient and his family. In S. Sherwood (Ed.),The hidden patient: knowledge and action in long-term care. New York: Spectrum Publications, 1975.
Miller, E.Abnormal ageing: the psychology of senile and presenile dementia. London: John Wiley and Sons, 1977.
Ross, H. E., & Kedward, H. B. Psychogeriatric hospital admissions from the community and institutions.Journal of Gerontology, 1977,32, 420–427.
Roth, M. The natural history of mental disorders in old age.Journal of Mental Science, 1955,101, 281–301.
Sainsbury, P., & Grad, J. Mental illness and the family.The Lancet, 1963,i, 544–547.(a)
Sainsbury, P., & Grad, J. Evaluating a community care service. In Freeman, H. L. and Farndale, J. (Eds.)Trends in the Mental Health Services: A Symposium of Original and Reported Papers. Oxford: Pergamon Press, 1963.(b)
Sainsbury, P. Evaluation of community mental health programs. In M. Guttentag & E. Struening (Eds.),Handbook of evaluation research. Beverly Hills, California: Sage Publications, 1975.
Sanford, J. R. A. Tolerance of debility in elderly dependents by supporters at home: Its significance for hospital practice.British Medical Journal, 1975,3, 471–473.
Savitsky, E., & Sharkey, H. The geriatric patient and his family: Study of family interaction in the aged.Journal of Geriatric Psychiatry, 1972,5, 3–19.
Shanas, E. & Maddox, G. L. Aging, health, and organization of health resources. In R. H. Binstock & E. Shanas (Eds.)Handbook of aging and the social sciences. New York: Van Nostrand Rheinhold, 1976.
Simon, A. A model for comprehensive mental health care for the aged. In A. Schwartz & I. Mensch (Eds.)Professional obligations and approaches to the aged. Springfield, Ill.: Charles G. Thomas, 1974.
Verwoerdt, A.Clinical geropsychiatry. Baltimore, Md.: Williams & Wilkins, 1976.
Wahl, P. R. Psychosocial implications of disorientation in the elderly.Nursing Clinics of North America, 1976,11, 145–155.
Wang, H. S. Dementia of old age. In W. L. Smith and M. Kinsbourne (Eds.),Aging and dementia. New York: Spectrum Publications, 1977.(a)
Wang, H. S. Organic brain syndrome In E. W. Busse and E. Pfeiffer (Eds.),Behavior and Adaptation in late life (2nd ed.). Boston: Little, Brown & Co., 1977.(b)
Lexical Access, Cognitive Psychology of
1.2 Connectionist Models of Lexical Processing
In the 1980s, the advent of connectionist modeling of word recognition processes led to a conceptualization whereby lexical information does not reside in a discretely defined entry.
In localist connectionist models (e.g., the Interactive-Activation account of McClelland and Rumelhart 1981 ), although there may be discrete units of activation that represent the words of the language, there are also units representing subword (i.e., sublexical) entities (e.g., letters). Sublexical activation is as integral to the recognition of the word as is lexical activation because there is an interaction between the sublexical and lexical levels in the determination of the output. In such a model, the process of matching the stimulus with a memory representation of the word involves not only the accessing of lexical information, but also sublexical information. Indeed, the whole word need not be represented at all, because its meaning could be activated solely via sublexical units (Taft 1991 ). So it is somewhat misleading, within this framework, to use the term ‘lexical access’ to refer to the actual matching process because it may not be based on lexical information, at least not exclusively. However, the term could be appropriately used to refer to the outcome of the matching process, namely the point at which information about the whole word is activated to some criterion of acceptability and is therefore ‘accessed.’
In distributed connectionist models (e.g., the Parallel Distributed Processing model of Seidenberg and McClelland 1989 ), the presented word activates a set of input units that produces a pattern of activation in a set of output units (via an intermediate set of hidden units) with no explicit lexical representation (see Cognition, Distributed ). This again obscures the idea of lexical access as a process of finding a sensory-to-lexical match. Nonetheless, at some point in processing, the system must settle on a particular output as being the most relevant to the input and, because this means that information about the word has become available for response, it could be argued that this is when ‘lexical access’ has occurred.
So, within connectionist accounts of word recognition, ‘lexical access’ refers most appropriately to the final outcome of processing rather than to the processing itself. The use of the term has therefore waned, because the central interest of cognitive investigations into word recognition is the nature of the actual processes involved in identifying a word and not the mere fact that the word is recognized. For this reason, the more general term ‘lexical processing’ tends to be preferred.
‘Warning Lights’ of Self-Righteousness
For many years, the Lord has been patiently and gradually showing me signs of the self-righteousness that hides in the deep recesses of my depraved heart. He began many years ago, and continues today. Sometime in the past year, a friend of mine gave me one of his extra copies of Extreme Righteousness: Seeing Ourselves in the Pharisees. This book is a biblical study of the Pharisees whom the author, Tom Hovestal, affectionately calls the “scoundrels” of the Gospel accounts. It has been in my “books to read soon” bag for awhile, but I finally took it out a few days ago. In the fourth chapter, the author effectively indicts every one of us as a Pharisee and warns of the self-righteousness that lurks within.
Pharisaism’s fatal flaw is self-righteousness. It lurks just beneath the surface of our evangelical souls. But we do not see it! Why? Perhaps we live such good lives that we look for sin in all the wrong places! We tune in to the external symbols of goodness but miss the internal symptoms of evil. Jesus does not want us, however, to live our lives in the pseudo-security of human righteousness. While on earth, He loved people too much to permit them to continue their merry religious ways blinded to their true spiritual condition. Instead He regularly engaged in the ministry of enabling religious people to find freedom and true life.
A few pages later, he writes, “We are sufficiently sophisticated and self-controlled to cover up most self-righteousness….So what subtle clues expose the hidden condition of our hearts?” He then describes 4 ‘warning lights of self-righteousness’ and challenges us to ask questions of ourselves. For myself, I see all four in my life at certain times and in varying degrees. How about you? Do you see yourself in this mirror?
Warning Light #1: A Contemptuous View of Others. “Do I compare myself with others and look down on those who do not live as I do? Of course, all the time! This tendency to compare my righteousness with others is endemic to humanity. Any level of contempt for others is a telltale sign of hidden self-righteousness.” The author then directs us to Luke 18:9.
Warning Light #2: A Shallow Sense of Forgiveness. “How deep and well-developed is my personal sense of God’s forgiveness? This subjective sense is another telltale symptom of my level of self-righteousness. Our personal awareness of God’s forgiveness will profoundly impact our level of self-righteousness. Our response to sinners, particularly those who wrong us, is an excellent gauge to measure potentially self-righteous hearts.” The author then directs us to Luke 7:36-50.
Warning Light #3: A Wrong Sense of Grace and Fairness. “How do I respond to working hard and being ignored when the less-deserving are rewarded and promoted? Fairness is a sense learned early in life in fact, fairness is one of the most well-developed senses of a child….But grace and fairness do not mix well. Grace by definition is unfair. It extends favor to the undeserving.” The author then directs us to the older brother in Luke 15:11-32.
Warning Light #4: An Unhealthy View of Failure. “How do I respond to failure or being exposed as a sinner?” The author then directs us to the parable found in Matthew 21:33-36.
When I think of Jesus being the Savior of self-righteous sinners, like me, I cannot help but think of the Apostle Paul’s conversion testimony in Philippians 3:7-11, which I relate to so well. The only way any of us can be saved is if we exchange our self-righteousness, which we mistakenly think we possess, for the righteousness of Jesus Christ, which can only be received as a gift by repentant faith. I am forever grateful for Jesus who died on the cross and rose again to save Pharisees like me.
In all, there were 4050 people with sufficient cognitive data to be classified into a subgroup. Demographic characteristics and average cognitive domain scores by study are shown in Table 1. Participants in the prospective cohort studies (ACT, MAP, and ROS) were older on average than those from ADNI and PITT. Most participants in each study self-reported white race (90% in ACT to 96% in MAP). There was some variation in cognitive performance across studies. The most notable differences from ACT (our reference for scaling) were for executive functioning in ADNI and ROS (average 0.8 units higher), and for language in MAP (average 0.8 units lower).
Proportions of people in each subgroup are shown in Fig. 1. There was considerable heterogeneity in proportions across studies (χ 2 df=20 = 468.7, p = 1.0 × 10 −86 ).
Proportions of people in each study and overall in each cognitively defined subgroup
Demographic characteristics of people in each subgroup were similar to those for people with Alzheimer’s disease overall (Supplementary Table 29). The proportion who were female ranged from 51% for isolated substantial relative executive functioning impairment to 63% of those with isolated substantial relative visuospatial impairment. Mean age at diagnosis ranged from 79 for those with isolated substantial relative visuospatial or memory impairment to 82 for those with isolated substantial relative language impairment. Mean years of education did not vary substantially across subgroups.
There were 3701 people with APOE genotype data (Table 2). We published APOE results from ACT  the proportion of those with isolated substantial memory impairment with ≥ 1 APOE ε4 allele was 12% higher than overall in that study. This finding was consistent across all five studies. Overall, the proportion of people with ≥ 1 APOE ε4 allele was 15% higher in those with isolated substantial memory impairment (65%) compared with the entire sample (50%). The differences in proportions with ≥ 1 APOE ε4 allele were highly significant (p = 1.5 × 10 −27 ). The APOE result was not sensitive to choosing other thresholds to indicate a substantial relative impairment (Supplementary Text 4 and Supplementary Fig. 2).
There were 2431 people with late-onset Alzheimer’s disease and 3447 cognitively normal elderly controls with genome-wide SNP data. Top results are shown in Fig. 2. There were 33 loci outside Chromosome 19 where the p-value for one subgroup was < 5 × 10 −5 . All of these had ORs < 0.77 or > 1.30 compared to cognitively normal elderly controls. These included nine loci for those with isolated substantial visuospatial impairment (red dots, including rs2289506 near NIT2 on chromosome 3, rs9369477 near SPATS1 on chromosome 4, rs2046197 near CSMD1 on chromosome 8, and rs8091629 near SLC14A2 on chromosome 18), nine for those with multiple domains with substantial relative impairments (yellow dots, including rs698842 near NRXN1 on chromosome 2, rs78872508 near HDAC9 on chromosome 7, and rs4348488 near BMP1 on chromosome 8), seven for those with no domain with a substantial relative impairment (purple dots, including rs11708767 near MED12L on chromosome 3, rs72839770 near DVL2 on chromosome 17, and rs7264688 near MGME1 on chromosome 20), six for those with isolated substantial language impairment (green dots, including rs13374908 near FAM163A on chromosome 1, rs28715896 near ERBB4 on chromosome 2, and rs75337321 near CACNA2D3 on chromosome 3), and two for those with isolated substantial memory impairment (blue dots, including rs1977412 near AGT on chromosome 1), and one for those with no domains with substantial impairments (purple dot, rs7264688 near MGME1 on chromosome 20). Other loci shown in Fig. 2 not named in the preceding sentence were > 50 kb from genes. Replication results are in Supplementary Tables 2a and 2b. All ORs were in the same direction for all these SNPs except rs28715896 on chromosome 2 near ERBB4, rs61835453 on chromosome 10, and rs365521 on chromosome 17. Heterogeneity p values did not suggest heterogeneity for any of these SNPs. No SNP outside the APOE region reached p < 5 × 10 −8 , the traditional level of genome-wide significance (Fig. 2).
Novel SNPs associated with cognitively defined subdomains with p < 10 –5 and OR < 0.77 or > 1.33. CAF=coded allele frequency. SNPs further than 50 kB from a gene do not have a gene name reported here. Gray shading in the odds ratios column of the figure delineates ORs > 0.77 and < 1.30, which is the range of ORs outside APOE from the International Genomics of Alzheimer’s Project (IGAP) 
Results for selected IGAP loci are shown in Supplementary Table 30. We selected subgroups with meta-analytic ORs < 0.77 or > 1.30 and for which results from all four data sets were in the same direction. Results for other IGAP SNPs for all studies and all subgroups are in Supplementary Table 31.
Across all datasets, there were 5878 people with SNP data who were either normal controls or Alzheimer’s disease cases. The logistic regression model for case vs. control status with age, sex, and IGAP gene scores had a likelihood of 176.13 and a pseudo-R 2 of 0.022. A model that included all of those terms and also included five subgroup gene scores had a likelihood of 311.94 and a pseudo-R 2 of 0.039. These were nested models we compared them with a likelihood ratio test with five degrees of freedom. The difference in likelihoods was highly significant (p = 1.39 × 10 −27 ).
The area under the ROC curve for the model with age, sex, and the IGAP genetic risk score was 0.60 (95% CI 0.58, 0.61), while for the model with age, sex, and five subgroup genetic risk scores, the area under the ROC curve was 0.62 (95% CI 0.61, 0.64). This difference was statistically significant (χ 2 df=1 = 11.15, p = 0.0008). Further analyses are described in Supplementary Text 12.
What are a digital dementia and a pseudo debility? - Psychology
RESEARCH STUDY INFORMATION
Information about research project:
Exploring how individuals who experience phenomena that have been described as ‘Conversion Disorder’ experience agency in their lives
as a requirement for a DCPsych in Counselling Psychology and Psychotherapy
from NSPC and Middlesex University
You are being invited to take part in a research study. Before you decide to participate, it is important for you to understand why the research is being done and what it will involve. Please take your time to read the following information carefully, and discuss it with others if you wish. Please ask if there is anything that is not clear or if you would like more information. Take your time to decide whether or not you wish to take part.
What is the purpose of the research ?
This study is being carried out as part of my studies at NSPC Ltd and Middlesex University. ‘Conversion disorder’ is a term used to describe specific types of bodily and sensory experiences, for example, seizures, disturbed balance, stuttering of speech, double vision, etc. Such experiences can involve feeling a lack of control over what is happening whereby one may feel as though they are no longer the agent of their own actions. The further exploration of how agency is experienced in a wider social and psychological context may serve to increase the understanding for both individuals and medical professionals. My study is designed to see how agency is experienced for individuals who have experiences described as ‘conversion disorder’. You are being asked to participate because you have replied to my advertisement for i) males who speak fluent English, ii) are 18 years old and above, iii) experience phenomena that have been described as ‘conversion disorder’, and iv) are able to read and understand the consent form as well as to participate in in-depth interviews. If however, you are i) a child, ii) an adult with a learning disability or dementia, iii) are currently self-harming and/or are suicidal, iv) have experienced a recent bereavement, or v) are intoxicated by a substance, you will be asked to refrain from participating in this research.
What will happen to me if I take part ?
I would like to initially have a brief conversation with you to see if this research is something that you may be interested in participating in and if so, then we could proceed to make an arrangement to meet so that you can undergo a single interview at a location that is convenient for us both, for example, a library or therapy room that has been hired out. The interview will last approximately one hour and will be audio-recorded. Should the interview take place over Skype it will be agreed beforehand that this take place in a suitable setting where confidentiality cannot be breached and no disturbances will take place. A qualitative research method approach called ‘interpretative phenomenological analysis’ will be used whereby your data will be analysed alongside other participants in order to discover how you experience agency and what it means for you to experience phenomena of ‘conversion disorder’.
What will you do with the information that I provide?
I will personally transcribe the audio recording and use a pseudo-name in place of your real name in order to ensure anonymity. I will transfer the files from the digital recorder to an encrypted computer and delete the files from the recorder. Any information that you provide me will be identified only with a project code and stored either on an encrypted USB stick or in a locked filing cabinet. I will keep the key that links your details with the project code in a locked filing cabinet.
For Skype-based interviews, I will carry out the necessary precautions to ensure that my private location will remain private at all times. It is important that you make the same arrangement for your own private location so as to ensure your privacy and any interruptions in the interview.
The information will be kept at least until 6 months after I graduate, and will be treated as confidential. If my research is published, I will make sure that neither your name nor other identifying details are used.
Data will be stored according to the Data Protection Act and the Freedom of Information Act.
What are the possible disadvantages of taking part?
In the interview I will ask you about your experience of phenomena described as ‘conversion disorder’ and your experience of agency (which is the extent to which you feel as though you are the agent of/in control of your life/world) involving this and other areas your life. However, talking about personal experiences may be distressing. If so, please let me know, and if you wish, I will stop the interview. Although this is very unlikely, should you tell me something that is required by law to pass on to a third person, (for example, child abuse, terrorism, money laundering), I will have to do so. Otherwise whatever you tell me will be confidential.
What are the possible benefits of taking part?
Being interviewed about your experience of phenomena described as ‘conversion disorder’ and agency has no direct benefit, either, although some people may find it an opportunity to reflect and could find this in itself beneficial. Should the research findings enhance the understanding of individuals and professionals involved so as to enable better communication, support and overall quality of life this would provide a possible benefit of taking part in the study.
You will be given a copy of this information sheet for your personal records, and if you agree to take part, you will be asked to sign the attached consent form before the study begins.
Participation in this research is entirely voluntary. You do not have to take part if you do not want to. If you decide to take part you may withdraw at any time without giving a reason and your data will be immediately destroyed.
Who is organising and funding the research?
The research is an entirely self-funded study.
Who has reviewed the study?
All proposals for research using human participants are reviewed by an Ethics Committee before they can proceed. The NSPC research ethics sub-committee have approved this study
If there are travel expenses, these will be fully reimbursed.
If you are interested in participating then please do not hesitate to contact me:
Head Case: Why Has PBS Promoted Controversial Shrink Dr. Daniel Amen?
Dr. Daniel Amen has built an empire on dubious brain imaging technology and nutritional supplements. (Illustration by Wesley Bedrosian for Observer)
Near the end of one of his many videos, which can be seen on your local public television station or YouTube, the psychiatrist Daniel Amen tells what he calls his “favorite story.” It has to do with his daughter, Breanne, who, Dr. Amen says with sadness in his voice, “I never thought was very smart.”
“One night,” Dr. Amen tells his rapt studio audience, “she came to me and she said, ‘Dad, I don’t think I can ever be as smart as my friends.’ And it broke my heart. Next day, I scanned her at the clinic.” This means that he subjected her to single photon emission computed tomography, or SPECT, which uses a radioactive isotope to measure blood flow in the brain. “And I’m like, ‘Oh my God!’ I cried when I saw this, because it indicated she had really low energy, really low blood flow in her brain.
“I knew how to fix it,” Dr. Amen continued. “The next day on just a little bit of targeted medication she was much better. Three months later , this girl who never got an A in her life, it was straight A’s! The next 10 years, straight A’s!”
It’s a sweet story, a clincher anecdote of the sort that has made Dr. Amen perhaps the best-known—as well as arguably the most controversial—psychiatrist in the nation. Over the years, he has built a psychiatric empire, with a chain of six Amen Clinics across the country, a steady stream of mega-selling books, a substantial media arm that produces programs shown on PBS member stations nationwide and a business promoting and selling proprietary nutritional supplements. It would be remarkable for any doctor to achieve the degree of notoriety that belongs to Dr. Amen. But what is perhaps most striking about his remarkable success is that it is built on claims, most notably the extraordinary, near-miraculous benefits of SPECT, which have been dismissed as medically worthless by a veritable who’s who of eminent, mainstream psychiatrists, neurologists and brain-imaging specialists.
Many neurologists question the value of SPECT scans. Facebook
SPECT is “spectacularly meaningless,” Daniel Carlat, professor of psychiatry at Tufts University, told The Washington Post in 2012. “Basically he’s conning people,” Jeffrey Lieberman, head of the psychiatry department at the Columbia College of Physicians and Surgeons, told me in a recent interview at Columbia Presbyterian Hospital, expressing a sentiment that I heard from at least a half dozen other specialists I interviewed at major universities and research institutions.
Dr. Amen “charges patients thousands of dollars to inject them with radioactive compounds and show them pretty colored pictures of their brains without any credible evidence that it adds to the diagnostic or treatment processes,” wrote Dr. Harriet Hall, a former Air Force flight surgeon and a prominent blogger on medical questions.
Dr. Amen is well aware of critiques like that, and he mounts an energetic defense: “I would offer that most of the people you talked to are not SPECT experts,” he told me in an email, “but rather experts in other imaging modalities, so they are unlikely to really know the scientific literature.” He also provided references to other experts who support his work and several studies that, he says, validate the claims that he has made. “We make diagnoses with all of the information, not just scans,” he said. “But when you add the scans, it changes what physicians do 8 times out of 10.”
Dr. Amen “charges patients thousands of dollars to inject them with radioactive compounds and show them pretty colored pictures of their brains without any credible evidence that it adds to the diagnostic or treatment processes,” wrote Dr. Harriet Hall.
But perhaps the most surprising thing about the prominence and celebrity (and wealth) that Dr. Amen has achieved over the past decade or so is the key, indispensable role played in his rise by the Public Broadcasting Service. Since 2008, a vast majority of the 350 PBS member stations across the country have regularly used one or another of Dr. Amen’s programs, almost always as part of their regular fundraising drives. A PBS spokesperson, Jan McNamara, told me, “PBS is not in a position to track and distribute data or comment on programming that we do not distribute.” But Dr. Amen told The Washington Post in 2012 that the number was around 50,000 total broadcasts—and no doubt the figure is much higher now.
“We broadcast Dr. Amen’s programs because they enjoy wide popularity among our viewers,” Kellie Castruita Specter, senior director for communications and marketing at Channel 13 in New York, wrote by email. “We understand that some medical professionals express reservations about his methods, and there are also some people who claim to have been cured by those same methods. Like many of the programs we carry, we broadcast them, and we allow the audience to judge for themselves.”
There would seem to be two questions in this sense. One has to do with the scientific-medical debate over the effectiveness of SPECT, and the claims Dr. Amen makes for his nutritional supplements, which many specialists dismiss as being nothing more than a 21st-century version of snake oil. The other issue has to do with the role PBS has played in giving both tremendous exposure to Dr. Amen as well as a stamp of approval that has the effect of validating his claims. Specter says that viewers can decide for themselves, but there seems little evidence that either PBS itself or the member stations that air his programs provide much in the way of information to enable viewers to make that judgment. The shows are both publicized and broadcast without a hint of the controversy surrounding Dr. Amen.
[youtube https://www.youtube.com/watch?v=4qRHM8N168w&w=560&h=315]The news here is that nothing has changed. Eight years ago when PBS stations began airing Dr. Amen’s programs, Robert Burton, M.D., the former chief of neurology at Mount Zion Hospital at the University of California in San Francisco, watched unbelieving as Dr. Amen told his studio audience, “I will show you how to make your brain great, including how to prevent Alzheimer’s disease.” Dr. Burton, sharing the consensus that there was no known, clinically proven way to prevent Alzheimer’s disease, subsequently complained on Salon that PBS “broadcast what amounts to an unregulated infomercial for Amen’s unproven treatments.”
Dr. Amen still claims that, using SPECT, he is able to detect Alzheimer’s disease years before symptoms occur and that he has a way of delaying its onset. “SPECT can change the Alzheimer’s epidemic,” he declared.
But several respected neurologists consulted by the Observer protest that there is no convincing evidence that this is true. “Even if the SPECT part of it was true, we absolutely don’t have any intervention to forestall the disease at this time,” said Dr. Howard Feldman, the director of the government-funded Alzheimer’s Disease Cooperative Study, whose purpose is precisely to test the effectiveness of new compounds and drugs. Meanwhile, paradoxically, Dr. Amen’s reputation, practice and businesses all continue to grow, enhanced by his continued appearances—with not a contrary word uttered on air—on PBS stations across the country.
Dr. Amen with a SPECT scanner at his Reston, VA clinic. (Photo: Joseph Victor Stefanchik - jvsstudios.com)
Daniel Amen is a slight, balding, 62-year-old with a friendly demeanor and a telegenic smile. He appears on his programs, which he produces in conjunction with High Five Entertainment in Nashville, talking in front of a studio audience. He usually wears a casual red knit pullover or a dark sports coat over a dark T-shirt, speaks eloquently and passionately, with just a tinge of valley girl syntax (“And I’m like, ‘Oh, my God!’ ”) to give him a common touch. He went to a small evangelical Christian college in California, spent three years in the Army after high school as an X-ray technician and received his medical degree from the now defunct Oral Roberts Medical School (the school’s namesake was an Elmer Gantry-like television evangelist).
“Psychiatry is the only specialty that doesn’t actually look at the organ it treats,” is a standard line he uses to introduce SPECT. “Imaging,” Dr. Amen said, “helped me see the underlying biology behind the symptoms.”
SPECT is mania with him. Over the years, he says, he’s accumulated the world’s largest collection of SPECT scans, with over 115,000 in his collection. After a young man has been dating one of his daughters for a few months, he makes the suitor undergo a SPECT scan. During all of his talks, he projects SPECT images on a screen. The healthy, “beautiful” brains are perfect ovals, cream-colored fading to violet and as smooth as marble. The “unhealthy,” diseased, traumatized brains are wrinkled and rumpled, a bit like hooked rugs. The brains of Alzheimer’s victims, a dramatic part of Dr. Amen’s presentations, are shriveled, riddled with holes they look like meteor fragments fallen to earth.
In fact, as brain-imaging specialists will tell you, actual brains, even the brains of Alzheimer’s sufferers, do not have gaping holes in them no living person’s brain is rumpled like a piece of corrugated metal. “He puts these images on screens in his talks without explanation, implying that this is a photographic likeness to the person’s brain,” Mark Slifstein, an associate professor in the department of psychiatry at Columbia University, told me. “It is not.”
But however Dr. Amen presents his scans, the more important point is the claims he makes for them. On Alzheimer’s, for example, he tells his studio audiences that the disease shows up in the brain 30 to 50 years before the onset of symptoms. Therefore, “You should be scanned early because treatment should be early.” He talks about former National Football League players suffering from brain damage, and he asserts that SPECT served as a crucial tool to diagnosing their injuries. He says that by putting these former players on a “smart program,” 80 percent of them were able to “rehabilitate their brains.” He boasts that SPECT images have enabled him to detect five specific brain patterns associated with being overweight. He contends that SPECT can help spot schizophrenia, depression and seven distinct forms of attention deficit hyperactivity disorder, or ADHD, and, since he can tailor his treatment to the type, he claims success in 9.5 out of 10 cases.
But these kinds of claims are exactly what arouse outrage from many brain specialists. Dr. Lieberman, a former president of the American Psychiatric Association, likens Dr. Amen’s use of SPECT to the 19th-century fad for phrenology, by which the size and shape of the skull were said to be measures of a person’s intelligence and personality. Dr. Amen’s use of those multihued images is “pseudo-color phrenology,” Dr. Lieberman charged. “What he does is present himself as practicing a new self-discovered form of psychiatry using a journeyman imaging technique—SPECT—to make diagnoses and select treatments,” he said. “There is absolutely no scientific evidence for what he says and does.”
“Theoretically it would be great if you could do a scan and use it to make a diagnosis,” Dr. Carlat of Tufts told me. “But the key point is that it’s all theoretical. There haven’t been any convincing studies at all that you can diagnose conditions that Dr. Amen says you can diagnose.” Dr. Carlat said he applauds Dr. Amen for some things, notably “bringing natural healing into his practice,” emphasizing things like nutrition, sleep and lifestyle as elements in psychological well-being. “But to the extent that he’s leading people to the false premise that you can use SPECT images to get a diagnosis, that’s where he verges on being a charlatan.”
PBS stations nationwide broadcast Dr. Amen’s videos. (Photo: YouTube)
SPECT technology uses a radioactive isotope injected into the bloodstream to measure blood flow in the heart or the brain. There was great excitement about the technology when it was first developed more than 30 years ago, but it was superseded and largely replaced by other scanning techniques, such as positron emission tomography (PET) or magnetic resonance imaging (MRI), which are both more advanced and, in the case of MRI, does not involve injecting radioactive materials into the bloodstream. Most specialists I talked to said it isn’t used much at all any more, though it is capable of helping to detect conditions like strokes, tumors and a rare form of Alzheimer’s disease known as front temporal dementia.
“It doesn’t have the resolution to give information pertaining to anything beyond these very dramatic conditions,” Dr. Lieberman said. “The images have zero relevance to mental disorders.”
“All of my career has been working with brain images of people with psychiatric conditions, including schizophrenia, depression, substance abuse, obsessive compulsive disorder, anorexia and bulimia, as well as people who do not have psychiatric conditions, and for the most part there are simply no visual differences among them,” Columbia’s Dr. Slifstein said. “The idea that you could diagnose any of these conditions in a single person by visually inspecting a SPECT blood-flow image is highly dubious.”
In 2010, two specialists at the Brain Imaging Council of the Society for Nuclear Medicine, Bryon Adinoff and Michael Devous, wrote in The American Journal of Psychiatry that several years earlier they had “offered to Dr. Amen the opportunity to submit his analyses of a blinded set of SPECT scans to determine how effective his technique is at correctly diagnosing subjects.” They said that in two decades, Dr. Amen never accepted that challenge, and yet “he has persisted in using scientifically unfounded claims to diagnose and treat patients.”
He contends that SPECT can help spot schizophrenia, depression and seven distinct forms of attention deficit hyperactivity disorder, or ADHD, and, since he can tailor his treatment to the type, he claims success in 9.5 out of 10 cases.
Asked about that, Dr. Amen told me by email, “I have never actually been asked,” though the text of the article in a major professional journal would seem to indicate that he has been asked. More generally, he argued that by sticking with SPECT and developing it, he has pioneered a diagnostic tool that the psychiatric establishment has been stubborn and foolish to ignore. “I have my share of critics,” he acknowledged, “but pressed on because our work changes lives, and that has always been the driving factor.” Moreover, he does have support among some other professionals—or he does up to a point. The Observer interviewed four doctors—psychiatrists or other specialists, all of them highly credentialed—whose names were provided by Dr. Amen, and all contended that SPECT is far more useful and far more promising than most specialists recognize.
“There is a lot of evidence that SPECT, if it is done with appropriate equipment and read by an appropriate reader, by measuring specific patterns of blood flow can be helpful in diagnosing dementia,” Andrew Newberg, a nuclear medicine specialist at Jefferson University Hospital in Philadelphia, explained by phone. Another specialist, Rob Tarzwell, a clinical assistant professor on the faculty of medicine at the University of British Columbia, co-authored a paper with Dr. Amen and Newberg showing that SPECT was useful in distinguishing between traumatic brain injury and post traumatic stress disorder (PTSD), a development that Discover magazine called one of the 100 top science stories of 2015.
“Ultimately, it doesn’t matter whether Dan’s specific patterns stand or fall,” Dr. Tarzwell concluded. “What matters is bringing a new diagnostic tool to maturity in psychiatry, where diagnostic tools are few and far between, and I think the discoveries Dan has made in a preliminary way are now on the cusp of being properly validated, or else properly refuted. It’s incredibly exciting.”
But while these specialists praised Dr. Amen, they all also acknowledged that he overstates his case, particularly on the television programs by which he spreads his message. They attribute this benignly to Dr. Amen’s sincere conviction that SPECT is vastly more beneficial than most experts realize.
Still, even his supporters stress what they describe as SPECT’s potential more than they do its established value. No expert that I talked to, for example, was convinced that SPECT can detect Alzheimer’s Disease years before the onset of symptoms, as Dr. Amen contends.
Dr. Amen has authored or co-authored numerous articles in professional journals, some of which he provided to me, presenting them as studies that confirm his claims. Among them, for example, is a recent paper in the Journal of Psychoactive Drugsshowing that in 30 cases of brain damage in former football players, a SPECT analysis combined with nutritional supplements produced “statistically significant increases in scores in attention, memory, reasoning, information processing, speed and accuracy.”
If that is true, it would be a major development, since what Dr. Amen is saying is that by using SPECT and his cocktail of nutritional supplements he has found an effective way to reverse brain damage. “Using all of our strategies, not just supplements, I sincerely believe and demonstrate in our clinics, that we can reverse brain damage,” Dr. Amen proclaimed by email. “I have shown it repeatedly.”
“Dr. Amen’s use of multihued images is ‘pseudo-color phrenology’…There is absolutely no scientific evidence for what he says and does.”—Dr. Jeffrey Lieberman, head of the psychiatry department at the Columbia College of Physicians and Surgeons
To his supporters, studies like the one on the football players, even if small, show at least that SPECT is an important, underutilized tool. What Dr. Amen’s critics don’t see, Dr. Tarzwell said, is that in the next five to 10 years, the resolution achieved by SPECT will improve greatly, and it will be able to do exactly what Dr. Amen said he does with it—see the physiology behind the psychological symptoms, detect disorders that don’t show up in the usual symptoms. “I’d rather have a guy like Daniel Amen overselling it than for us to just shout into the abyss,” he said.
But while the study showing such good results in reversing brain damage might convince a lay audience watching PBS, professionals maintain that it has no scientific validity or clinical value, mainly because it was done with no control group, so it is impossible to know whether the improvements measured by Dr. Amen were due to SPECT and supplements or to a placebo effect, which is often very powerful.
“Normally you would evaluate a person without SPECT and then do an evaluation with SPECT and show a difference, but that’s not what was done in this case,” a senior scientist at the National Institutes of Health who requested anonymity told the Observer. “They don’t show that SPECT was any better than good clinical judgment.” The damage-reversal study was an open-label one, meaning that the former football players who were its subjects knew that they were taking supplements and not a placebo. “Nothing can be concluded from such studies,” Dr. Paul Aisen, a neurologist at the Keck School of Medicine at USC and one of the country’s leading Alzheimer’s researchers, concluded after reviewing the studies that Dr. Amen had shown the Observer. “They show no meaningful evidence in favor of SPECT scanning or nutritional supplements.”
One of many supplements Dr. Amen sells on his website. (Screenshot from Facebook)
And then there are those nutritional supplements themselves, which Dr. Amen sells online, claiming that they benefit healthy people as well as brain-damaged ones, but here even the people he designated to speak on his behalf expressed skepticism. “I don’t use supplements in my practice,” Dr. Tarzwell said. “There isn’t much data in terms of large, randomized trials,” Dr. Newberg told me, speaking of supplements in general. “That’s in part because many doctors are biased against supplements, but even so there are small studies showing potential benefits.”
Dr. Amen himself is vague in his television programs on what exactly he prescribes for patients—using phrases like “targeted medication,” “dopamine boosters” or “smart programs,” rather than specify exactly what medication his patients are taking. But as his study of football players shows, he relies a great deal on supplements, more or less like the “BrainMD” products he promotes and sells on his website—consisting of substances like multivitamins, ginkgo biloba extract, omega-3 fatty acids, a moss extract known as Huperzine A and another 50 or so ingredients. “This is one of the best brain health supplements available,” Dr. Amen exclaims on his website, “offering support for a wide range of cognitive functions, including focus, memory and mental clarity.”
There’s always some buzz about one or another supplement—remember the Nobel Laureate Linus Pauling’s claims for vitamin C, or the belief that garlic pills will keep you healthy. Over the years, scientists at research institutes have tested substances like St. John’s Wort for depression and ginkgo biloba and Huperzine A for Alzheimer’s Disease. Dr. Amen seems especially fond of ginkgo, saying in one of his programs, “The prettiest scans I’ve ever seen are from people who take ginkgo.”
But the experts who find his SPECT claims unfounded feel the same way about his supplements. Dr. Aisen of USC recalled, for example, a study of ginkgo extract that showed some possible benefit in slowing Alzheimer’s, but, he said, “the study wasn’t replicated, and nobody I know would prescribe it.” More generally, Dr. Aisen said, “There is no study showing any benefit of any of these things in normal people.”
“A lot of them have been tested,” Dr. Feldman of the Alzheimer’s Disease Cooperative Study told me, referring to the ingredients in Dr. Amen’s BrainMD product. “Unfortunately none of them has withstood the test of clinical effectiveness.”
The way Dr. Amen’s programs are presented and used by PBS amount to an unqualified, if implicit, endorsement.
But that’s the sort of expert opinion you won’t see on PBS. Indeed, the way Dr. Amen’s programs are presented and used amount to an unqualified, if implicit, endorsement of Dr. Amen himself and his claims. The stations, for example, give away his books and videos in exchange for donations. For $90, you get a DVD of the pledge program plus a copy of Dr. Amen’s best-selling book, Change Your Brain, Change Your life: The Breakthrough Program for Conquering Anxiety, Depression, Obsessiveness, Lack of Focus, Anger, and Memory Problems. For a $240 pledge, the gift is the book plus Dr. Amen’s Change Your Life DVD.
Dr. Amen “gives very specific steps to boost your mood, focus and memory and decrease your risk for Alzheimer’s Disease,” intoned the publicity that KCTS in Seattle put out on its website this spring in advance of airing Dr. Amen’s newest program. I saw the KCTS broadcast, which was accompanied by a separate interview with Dr. Amen that can only be described as fawning. (Efforts to get someone at the station to comment were unavailing.) And then there’s always that tagline reiterated at some point by the station host: “This is the kind of programming you can only get on PBS.”
Dr. Amen told me that he receives “a small percentage, less than 25 percent” of the donations received by the stations airing his programs, which, he said, covers his production and distribution costs. That’s a pretty good deal. The PBS stations, limited in the amount of advertising they can sell directly, depend on member donations, which they use for such quality programs as Nova, Frontline and others. By using Dr. Amen’s programs for fundraising they are engaging in a kind of indirect advertising, during which Dr. Amen, in his hour-long studio appearances, can promote himself, his methods and, indirectly, his nutritional supplement business without having to label this promotion as advertising or to suffer any contrary opinions.
These services and products, moreover, don’t come cheap. An initial consultation at one of Dr. Amen’s clinics costs $400. A SPECT examination, consisting of two scans, one at rest and one while concentrating, costs $3,950, which most medical insurance does not cover. During a visit to Amen Clinics’ New York branch, I was told that 85 to 90 percent of patients elect to have SPECT scans, with many of them first hearing about the technique on PBS. Dr. Amen’s mid-range nutritional supplement, called “Brain and Body Power,” sells for $84.96 a month if you elect automatic monthly shipments.
This spring, stations from WNET in New York to KPBS in San Diego broadcast Dr. Amen’s latest video, On the Psychiatrist’s Couch, whose refrain is, “You’re not stuck with the brain you have you can make it better.” In the advance publicity on their websites, these stations frequently cite a 2012 article in The Washington Post to the effect that “Daniel Amen is the most popular psychiatrist in America.” The publicity neglects to mention the second half of the headline on what was actually a highly critical Washington Post profile: “To most researchers that’s a very bad thing.”
Richard Bernstein, a former reporter and critic at The New York Times, is the author of China 1945: Mao’s Revolution and America’s Fateful Choice. Follow him on twitter: @R_Bernstein
Using Reality Orientation in Alzheimer's and Dementia
Claudia Chaves, MD, is board-certified in cerebrovascular disease and neurology with a subspecialty certification in vascular neurology.
Reality orientation has its roots in a technique used with disabled veterans to help them engage in, and connect with, their surroundings. It's an approach where the environment, including dates, locations, and current surroundings, is frequently pointed out and woven into the conversations with the person. Reality orientation, when used appropriately and with compassion, can also benefit those living with Alzheimer's disease and other dementias.
The tools for reality orientation aim to reinforce the naming of objects and people as well as a timeline of events, past or present. This typically involves:
- Talking about orientation, including the day, time of day, date, and season
- Using people's name frequently
- Discussing current events
- Referring to clocks and calendars
- Placing signs and labels on doors, cupboards, and other objects
- Asking questions about photos or other memorabilia
The functions of the vagus nerve
The vagus nerve controls the parasympathetic system. It intervenes in many functions, from mouth movements to heartbeat, and likewise, when affected it can cause various symptoms. Some of the vagus nerve functions in our body are:
– It helps regulate heartbeat, controls muscle movements and maintains the pace of breathing.
– It maintains the functioning of the digestive tract, allowing the contraction of the stomach and intestine muscles to digest food.
– Facilitates relaxation after a stressful situation or indicates that we are in danger and we do not have to lower the guard.
– Send sensory information to the brain about organ status.
Dementia Symptoms, Causes, Types, Stages, and Treatments
Dementia is a syndrome characterized with signs and symptoms like:
- Impairment in memory, impairment in another area of thinking such as the ability to organize thoughts and reason, the ability to use language, or the ability to see accurately the visual world (not because of eye disease).
- These impairments are severe enough to cause a decline in the patient's usual level of functioning. Although some kinds of memory loss are normal parts of aging, the changes due to aging are not severe enough to interfere with the level of function.
- Although many different diseases can cause dementia, Alzheimer's disease is the most common cause for dementia in the United States and in most countries in the world.
What is dementia?
Dementia is often one of the most misunderstood conditions in medicine today. Some people believe that senility or senile dementia is an inevitable result of aging, and never seek evaluation for family members who show signs of memory loss. Others believe that any evidence of forgetfulness is evidence of dementia. Neither of these conclusions is accurate.
Additionally, many questions have been raised about dementia. Does dementia differ from Alzheimer's disease or are all forms of dementia Alzheimer's disease? If someone has memory loss associated with another condition, does that turn into Alzheimer's disease? What can be expected if someone has been diagnosed with dementia?
What are the early and later signs and symptoms of dementia?
Early signs of dementia may include:
- Simple forgetfulness
- Losing items
- Problems performing tasks or activities that were previously done without effort.
- Difficulty with learning new material is frequently one of the earliest signs of dementia.
Many patients with early Alzheimer's disease or other types of dementia are unaware that they have any problem. As the disease progresses, behavioral changes can become evident.
- Patients have difficulty performing basic tasks, such as getting dressed or using the bathroom.
- Some patients begin to forget pieces of information about themselves, including their address or telephone number, or even their date of birth.
- They may have difficulty understanding what is occurring around them.
- Some patients have problems remembering to eat and may develop pronounced weight loss.
- In the late stages of dementia, patients often cannot recognize family members and their ability to communicate effectively is markedly impaired.
- They are no longer able to effectively care for themselves and require assistance for all activities of daily living.
- Over time, patients can forget how to walk or even how to sit up.
What causes dementia?
Dementia is a broad term which covers many different conditions, including Alzheimer's disease, vascular dementia, frontotemporal dementia, and other disorders.
- Simple forgetfulness is not enough to lead to a diagnosis of dementia, as there needs to be evidence of problems in at least two areas of cognition (brain function) to confirm this diagnosis.
- Possible symptoms or signs of dementia include:
- Memory loss.
- Problems with speaking including difficulty completing sentences or finding the right word to say
- Difficulty completing tasks.
- Difficulty recognizing items or people.
- Showing signs of poor judgment.
- People with dementia may have problems preparing food.
- Performing household chores
- Paying bills.
They may repeat questions or stories regularly, or forget appointments. They may get lost in familiar environments. Personality changes, including irritability or agitation, may also occur. In some cases, people with dementia develop hallucinations (or see things which aren't really there).
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What are Alzheimer's, vascular, and frontotemporal dementia?
- Alzheimer&rsquos dementia/Alzheimer&rsquos disease (AD) is the most common form of dementia. The cause has not yet been identified. While patients with AD have amyloid plaques (an accumulation of an abnormal protein) identified in certain areas of their brain, it is unclear if these plaques are the cause of the disease or a result of the disease. Although most cases of Alzheimer's disease begin after the age of 65, in some cases symptoms begin when someone is in their 40s or 50s. This early onset Alzheimer's disease can progress more rapidly than later onset AD.
- Vascular dementia is the second most common cause of dementia, and is due to multiple strokes occurring within the brain. Often, these strokes may have been unnoticed and patients may not have any associated symptoms such as weakness, visual loss, or numbness. Patients with untreated high blood pressure or heart disease may be at risk of developing vascular dementia.
- Frontotemporal dementia is associated with pronounced atrophy or shrinkage of the frontal and temporal lobes in the brain. In addition to forgetfulness and word finding problems, patients may have marked personality changes, impulsivity, or poor judgment. Some patients with frontotemporal dementia can develop incoordination or stiffness of their muscles.
What are hydrocephalus, alcoholic, Hunington's, and trauma dementia?
- Normal pressure hydrocephalusis an abnormal enlargement of the ventricles, or fluid filled spaces within the brain, that causes pressure on areas of the brain. This leads to problems with walking, memory, and ability to control urine flow (incontinence). Although this can be identified with imaging of the brain (MRI or CT scan), further testing may be required to confirm the diagnosis. If diagnosed, this condition can be treated with placement of a shunt to drain the extra fluid.
- Huntington&rsquos disease causes characteristic abnormal movements, called chorea, in affected individuals. The movements are the hallmark of the diagnosis. However, in some cases, problems with memory can precede the development of the chorea by many years.
- Alcoholic dementia is caused when patients drink heavily and develop deficiency in one of the B vitamins. When this happens, brain cells are unable to function normally and memory loss can occur. This is called Korsakoff syndrome. Although it is most commonly seen in alcoholics, patients who are malnourished from other causes are also at risk of developing this disorder.
- Traumatic brain injury (concussion)/dementia) pugilistica can lead to memory problems, as we have learned in recent years. In some cases, recurrent brain injuries or repeated concussions can contribute to the underlying changes identified in Alzheimer's disease.
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What are Lewy body, Creutzfeldt-Jakob, and mixed dementia
- Lewy body dementia/Lewy body disease is caused by Lewy bodies, which are abnormal clumps of certain proteins, accumulating inside of neurons. Forgetfulness and other signs of cognitive decline are the primary features of this condition, but patients can also develop prominent hallucinations which seem very real to them. Some patients with Lewy body disease develop symptoms which look like Parkinson's disease, such as tremor and slowness.
- Creutzfeldt-Jakob diseaseis a rare condition where an abnormal protein leads to destruction of brain cells and dementia. While most cases occur without an underlying cause, in some patients there is a family history of this disorder. Even less often, patients might be exposed to the abnormal protein. Mad cow disease is one example of external exposure. This condition tends to progress rapidly, over only a few years, and is often associated with abnormal muscle movements.
- Mixed dementia refers to patients who have evidence of two (or more) types of dementia. They are often described as having mixed dementia. Alzheimer's disease and vascular dementia are the most common causes of mixed dementia.
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What are the stages of dementia?
The stages of dementia are loosely grouped into mild, moderate, and severe categories by some doctors. However, there is another system of staging for dementia.
- Stage 1: No cognitive decline.
- Stage 2: Mild cognitive decline.
- Stage 3: Moderate cognitive decline, for example, dementia impairment like memory lapses, and losing objects daily.
- Stage 4: Moderately severe cognitive decline, for example, poor short-term memory, forgetting personal details, and difficulty with basic math. This is usually is the longest stage of dementia.
- Stage 5: Moderately severe cognitive decline, for example, increasing problems planning or organizing, disorientation, and may no longer be able to live alone.
- Stage 6: Severe cognitive decline, for example, problems recognizing friends and family members, and memory loss that worsens.
- Stage 7: Very severe cognitive decline. This is the final stage of dementia. Body systems decline, and communication is limited.
Patients may seem to fall into two different stages at the same time, depending on what symptoms they are experiencing. The different stages of dementia cannot be used to predict how rapidly someone's condition might progress and patients may remain in one stage for many years or for only a few months. Every patient has a different progression of their disease.
What are the risk factors for dementia?
The risk factors for developing dementia include age and family history. Age and a family history of dementia are non-modifiable risk factors. Abnormal genes which are associated with Alzheimer's disease have been identified, but are only rarely involved in the development of Alzheimer's disease. Conditions such as high blood pressure, high cholesterol, or diabetes increase the risks of developing either Alzheimer's disease or multi-infarct dementia. Some medications can lead to memory problems which look like dementia.
How is dementia diagnosed?
To diagnosis dementia, testing is performed by doctors. While in-office screening assessments are sometimes enough to confirm a diagnosis, at other times a more in-depth evaluation is required. Blood testing and imaging studies are often completed to confirm that reversible conditions such as thyroid disease or certain vitamin deficiencies are not present.
What is the treatment for dementia?
Treatment options for Alzheimer's disease and other dementia are limited. While there are medications available to try to improve the symptoms of Alzheimer's disease, the effect of these medications is limited. Physical exercise has been shown to be of some benefit in helping to maintain cognition. Staying engaged and participating in social events may also be of some help. To date, no treatment which can reverse the process of Alzheimer's disease has been identified.
What is the life expectancy for dementia? Can it be cured?
There is no cure for dementia.
- Although Alzheimer's disease is listed as the 6th most common cause of death in the U.S.. Patients with Alzheimer's disease most commonly die due to infections caused by lack of mobility. , bladder infections, bedsores, and other causes can lead to more wide-spread infection and subsequent death.
- Patients with dementias have widely varying life expectancies, depending on the underlying cause of their dementia. Life expectancy can range from only 1 to 2 years to more than 15 years the average duration of the disease is between 4 and 8 years after diagnosis.
How can you cope with being the caretaker of someone with dementia?
It is important for someone who is the primary caregiver of a patient with dementia to have a strong network of support. This is needed both to aid in caring for the patient and to give the caregiver some intermittent relief. In the early stages, many caregivers function more as a helper or guide, providing reminders for different tasks. Later in the disease, caregivers may have to supply basic care to the patient, including assistance with bathing, dressing, and going to the bathroom.
Obtaining power of attorney status for financial and medical matters and determining when a patient is no longer able to perform certain activities, such as driving, are difficult but necessary actions. Local Alzheimer's Association chapters are often helpful in completing these tasks. Enlisting the help of a patient's physician or mandating an on-the-road driving assessment can place the responsibility of determining when a patient is no longer safe to drive on someone other than a caregiver or family member, as driving is often an action that many patients attempt to perform far past the time when it is safe to continue. There are many sources of assistance for caregivers of patients with dementia:
Alzheimer's and Dementia Caregiver Center
Can dementia be prevented?
While there is no way to absolutely prevent the development of dementia, different activities have been identified which might decrease the risk. These include maintaining optimal health, including normal blood pressure, normal cholesterol, and normal blood sugars. Staying physically active, avoiding tobacco use or excess alcohol intake, maintaining a healthy weight, and preventing head injuries are also recommended.