Saturday, 20 February 2016

Time for the second opinion

Since being referred for a second opinion for Lewy Body Dementia in September,  I have been waiting to the results of tests to come through so we can get the answers.

It's taken some time to get this far, but as a second specialist has now been in touch about a follow up appointment for my balance/ "Parkinson" issues, and  we found out the some results had not been forwarded to the correct place.

This morning my wife spoke to a medical secretary about this, and we have now been given an appointment date for early next month.

I confess that I am getting very nervous about this, but I am hopeful that this can now be resolved and we can move in with our lives,

It may be that more tests may be required, but at least things are now moving.

I have never been sure that I had a form of dementia, but recognised that I do have memory , balance and tremor problems at times. 

This short term memory has caused a lot of problems, and it got to the stage where I refused to get involved with discussions or meetings, because I could not always remember what had just been said. 

 My hobby of photography has also suffered over the last two years, and that is something I got a lot of pleasure out of doing, but when you struggle with the camera settings, you lose interest

This also caused problems when replying to emails, because I cannot remember what has been written, and sometimes repeat myself. 

This sometimes causes me to repeat things that have already been spoken about by other am and that is embarrassing to me as well as to others, 

I sometimes get very annoyed when I am trying to do simple DIY tasks, because I don't always remember how to do these anymore, even though I have done them all of my working life. 

If I ever manage to complete one of these tasks properly, I feel as if I have won the Lottery, and get a sense of achievement. But sadly those days are few and far between.

I know that I have brain shrinkage because it was picked up in an MRI scan, buts that's as much as I know.

So I am now just waiting to see if we can get any further forward with this diagnosis. 

My problem is that I forget things so easily, that when it comes to appointments, it all goes out of the window, and I struggle to remember.

My wife has said that I am going to have to sit down and try to write things out, before I have my next appointment. 

This would help me and also the doctor I am seeing, but it's easier said than done at times, because unless I write it down fast, it's gone for ever



Skin Test Project to Aid LBD Diagnosis

Skin Test Project to Aid LBD Diagnosis
α-Synuclein biopsy project
Background
Dementia with Lewy bodies (DLB) is the second most common type of neurodegenerative dementia after Alzheimer’s disease. It is associated with characteristic features such as the symptoms of Parkinson’s disease, visual hallucinations and fluctuating cognitive impairment. The diagnosis of DLB can be difficult. Currently there is a scan that helps to diagnose DLB, but it is negative in around 1 in 5 people who have DLB. In the earliest stages of the disease, this scan may be less useful.
DLB and Parkinson’s disease (PD) are part of a group of illnesses called Lewy body disorders. These are cause by deposition of a protein called α-synuclein in the brain. α-synuclein is also found in other parts of the body, such as the nerves in the skin and gut.
Identifying α-synuclein in areas outside the brain may help in the diagnosis of DLB and PD. Earlier diagnosis could be possible because α-synuclein may be present in these areas before it is present in the brain. Recently, a study used a new technique to reliably identify α-synuclein in the skin of people with PD using a test called punch biopsy. The punch biopsy has been described as a safe and minimally invasive technique by the European Federation of Neurological Societies.
The Punch Biopsy
The sample is taken from arm or leg
A local anaesthetic is used to numb the skin. This stings a bit, but the skin should then be numb for the procedure.
A small sample is taken as shown in the diagram. The actual width of the sample taken is the same as this dot:
A single suture may be inserted at the site. This will be removed a few days later by the study team.
Aims
We would like to test if α-synuclein can be found in the skin of people with DLB. If α-synuclein is found to be present in DLB, punch biopsies may be a useful tool in the diagnosis of DLB, particularly in the earliest stages of the disease.
Participants will already have a diagnosis of DLB or AD or will be healthy control subjects. The procedure will not benefit them directly. The aim of the study is to see if punch biopsies could be used to help diagnose DLB in the future.


Thursday, 11 February 2016

The Connection Between Dementia and Chronic Lung Disease

24 Mar 2015 | Under COPDLung DiseaseRelated Conditions | Posted by rmsadmin | 8 Comments
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Acknowledging the Dementia Epidemic
Currently, we live in a society that constantly hears about the presence of Alzheimer’s disease and dementia. Between popular culture promoting films such as Still Alice and Away From Her and the increased effort to find a cure, people are finally beginning to care about these debilitating conditions. Just this past week at a World Health Organization (WHO) conference, a global action called for increased investment (over 100 million dollars) in promising research efforts for dementia. With the aging population, the WHO Director General said:
“There is a tidal wave of dementia coming our way worldwide…we need to see greater investments in research to develop a cure, but also to improve the quality of life of people living with dementia and the support given to their caregivers.”
In many ways, the first step in curing dementia is learning how it develops and certain risk factors that contribute to a dementia diagnosis. Recent studies point to a link between chronic lung diseases like COPD and the development of dementia.
An Introduction to COPD and Other Chronic Lung Diseases 
Chronic obstructive pulmonary disorder (COPD) is a progressive lung disease that restricts the airflow in and out of the lungs. As a result, sufferers of a chronic lung disease like COPD often experience shortness of breath, wheezing, coughing and the inability to perform simple tasks. Oftentimes, sufferers have very low oxygen levels, which can result in brain damage due to a lack of oxygen to the brain.
Scientific Findings about Lung Function and Cognitive Decline
Researchers began studying the connection between lung function and dementia risk in the 90’s. Ever since, new studies have emerged that point a finger at an increased risk for memory loss and dementia resulting from impaired lung function and chronic lung disease. Just in 2011, a fifteen-year study supported the hypothesis that reduced lung function increased the risk for dementia. The over-a-decade long study included 10,975 individuals and repeated pulmonary function tests and cognitive assessments. In the end, it is confirmed that lung function greatly impacts cognitive ability.
One study called Cognitive-pulmonary Disease states that “patients with COPD may have cognitive impairment, either globally or in single cognitive domains, such as information processing, attention and concentration, memory…” It is suspected that the cause is from hypoxemia, which is low blood oxygen levels, hypercapnia (an increased amount of carbon dioxide in the blood—a common side effect of smoking and COPD), or structural brain damage, such as the loss of white matter integrity, which can be induced by smoking.
As a result of new research findings, scientists are looking into the relationship between smoking and cognitive ability and the relationship between COPD and dementia. Due to the strong correlation between all three, we wonder whether quitting smoking could not only decrease your chances of developing COPD or another chronic lung disease, but could it decrease your chances of developing dementia as well? It is hoped that future research will determine whether maintaining optimal pulmonary health could prevent the development of dementia or Alzheimer’s disease. Perhaps even more intriguing is the possibility that treating your chronic lung disease could not only improve your lung function and quality of life, but it could also help maintain healthy cognition.
Improving your Lung Function
The benefits of improving your lung function seem relatively obvious: the ability to breathe easier, the chance to get back to the life you want, an improved prognosis—the list goes on. Now, there is the potential for improved lung function to also decrease the likelihood of developing a debilitating condition like dementia. Unfortunately, chronic lung diseases are incurable, but that does not mean they are untreatable. The Lung Institute is dedicated to challenging the incurable with regenerative medicine. Sufferers of a chronic lung disease can improve their lung function with stem cell therapy. For more information, visit us at lunginstitute.com or call us at (800) 729-3065.



COPD Linked to Cognitive Impairment

COPD Linked to Cognitive Impairment and Memory Loss
Laurie Barclay, MD
December 12, 2013
·         Add Other Topics
·         Emphysema Imaging
Chronic obstructive pulmonary disease (COPD) was associated with increased odds of having mild cognitive impairment (MCI) and memory loss in a cross-sectional, population-based study. The study, published in the November issue of the Mayo Clinic Proceedings, also showed a dose–response relationship with COPD duration and increasing risk for cognitive problems.
"In the absence of any effective therapy for dementia, the identification of risk factors for the development of MCI may hold the best promise for preventing or delaying the progression of early cognitive changes to clinical dementia," write Balwinder Singh, MD, from Mayo Clinic in Rochester, Minnesota, and colleagues.
"Recent studies suggest that up to 77% of patients with both COPD and hypoxemia have some form of cognitive impairment. However, few well-designed population-based studies have examined the association between COPD and MCI."
Therefore the researchers looked for an association between COPD and MCI and MCI subtype (amnestic or nonamnestic), in the population-based Mayo Clinic Study of Aging, using data from October 1, 2004, through July 31, 2007. Participants were aged 70 to 89 years and underwent a nurse assessment, neurological evaluation, and neuropsychological testing at study entry.
Using standardized criteria, a consensus panel diagnosed MCI, and the researchers reviewed medical records to identify individuals with COPD. Logistic regression models adjusted for potential covariates allowed evaluation of the associations of COPD and disease duration with MCI and its subtypes.
Of 1927 participants, 288 had COPD, which included 18% of men and 12% of women (P < .001). Prevalence of MCI was significantly higher in patients with COPD (27%) than in patients without COPD (15%; P < .001). The odds ratio (OR) for MCI was nearly double in those patients with COPD compared with those without COPD (OR, 1.87; 95% CI, 1.34 - 2.61). Findings were similar in both sexes.
In addition, COPD was associated with almost 2-fold higher odds of amnestic MCI (characterized by memory loss), but not with nonamnestic MCI. However, the study authors suggest that the nonsignificant association of COPD with nonamnestic MCI could be a result of reduced power on data stratification.
The associations of COPD with overall MCI and amnestic MCI were independent of age, sex, education, apolipoprotein E genotype, body mass index, depression, and a history of diabetes, hypertension, coronary artery disease, and stroke.
Dose–Response Effect for COPD Duration
There appeared to be a dose–response effect for COPD duration, with an OR for MCI of 1.60 (95% CI, 0.97 - 2.57) in patients with a COPD duration of 5 years or less and 2.10 (95% CI, 1.38 - 3.14) in patients with a COPD duration exceeding 5 years.
"This population-based study suggests that COPD is associated with increased odds of having MCI and its subtypes," the study authors write. "There was a dose-response relationship with the duration of COPD after controlling for the potential covariates."
Limitations of this study include its cross-sectional design, precluding causal inferences; reliance on physician diagnosis of COPD as recorded in medical records; and a primarily white population, which may limit its generalizability. The investigators recommend additional longitudinal studies in population-based cohorts to determine whether COPD is in fact associated with risk for incident MCI and dementia.
"COPD is reversible in early stages, especially in smokers," Dr. Singh said in a Mayo Clinic news release. "These findings are important because they highlight the importance of COPD as a potential risk factor for MCI and will hopefully lead to early intervention to prevent incidence or progression."
The National Institutes of Health (NIH), the Robert Wood Johnson Foundation, the Robert H. and Clarice Smith and Abigail van Buren Alzheimer's Disease Research Program, the National Center for Advancing Translational Sciences from the NIH, and the Rochester Epidemiology Project funded this study. Some of the study authors reported various financial disclosures involving the National Institute on Aging, the Alzheimer Drug Discovery Foundation, the NIH, the Driskill Foundation, BI, Merck, Forrest, the Alzheimer's Association, the National Advisory Council on Aging, Elan/Janssen AI, Pfizer Inc (Wyeth), GE Healthcare, Oxford University Press, and/or NIH/National Advisory Council on Aging.
Mayo Clin Proc. 2013;88:1222-1230. Full text


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