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Health News from NHS Choices

Constantly updated health news across a range of subjects.

NHS Choices News

  • Are good neighbours really life-savers?

    “Having good neighbours can help cut heart attack risk,” reports The Independent.

    The paper reports on a nationally representative US study of over 5,000 adults over the age of 50.

    People were asked about how they rated their neighbourhood social cohesion, then followed up for four years to see if they had a heart attack.

    Social cohesion refers to how “neighbourly” people feel, and relates to feelings of security, connection to the area and trust of inhabitants. In this study, social cohesion was assessed by asking people how much they agreed with simple statements such as “people in this area are friendly” and “people in this area can be trusted”.

    The study found that higher social cohesion was associated with a reduced risk of heart attack.

    However, the association became non-significant (could have been the result of chance) once the researchers adjusted for all factors known to be associated with heart attack risk, such as smoking history, exercise and body mass index (BMI).

    This makes it more difficult to draw any meaningful interpretation from these results. It's likely that any link between the risk of a heart attack and perceived social cohesion is being influenced by a varied mix of other factors.

    While building social connections can bring mental health benefits, relying on your neighbours to cut your risk of a heart attack is probably unwise.

     

    Where did the story come from?

    The study was carried out by researchers from the University of Michigan. Sources of funding were not reported. 

    The study was published in the peer-reviewed Journal of Epidemiology & Community Health.

    This story was covered by The Independent, the Mail Online and The Daily Telegraph.

    It was not stated that the association between social cohesion and heart attack was no longer significant when all covariates were adjusted for.

    However, the Telegraph did make the point that it is too early to make any definitive conclusions.

     

    What kind of research was this?

    This was a cohort study that investigated whether higher perceived neighbourhood social cohesion was associated with lower incidence of heart attack (myocardial infarction).

    Cohort studies cannot show that higher social cohesion caused the reduction in heart attacks, as there could be many other factors responsible for any association seen.

     

    What did the research involve?

    The researchers analysed 5,276 people without a history of heart disease who were taking part in the Health and Retirement Study – a nationally representative study of American adults over the age of 50.

    People were asked at the beginning of the study about how they rated their neighbourhood social cohesion. Social cohesion was measured by the participants’ agreement with the following statements:

    • “I really feel part of this area”
    • “If you were in trouble, there are lots of people in this area who would help you”
    • “Most people in this area can be trusted”
    • “Most people in this area are friendly”

    There was then a follow-up period of four years to see if those studied had a heart attack, which was self-reported or reported by a proxy if the participant had died.

    The researchers looked to see if people with higher perceived social neighbourhood cohesion had a reduced risk of heart attack.

     

    What were the basic results?

    During the four-year study, 148 people (2.81%) people had a heart attack.

    Each standard deviation (a measure of variation from the average) increase in perceived neighbourhood social cohesion was associated with a 22% reduced odds of heart attack after adjusting for age, gender, race, marital status, education and total wealth (odds ratio [OR] 0.78, 95% confidence interval [CI] 0.63 to 0.94).

    However, the association was no longer statistically significant if all potential confounders were adjusted for (age, gender, race/ethnicity, marital status, education level, total wealth, smoking, exercise, alcohol frequency, high blood pressure, diabetes, BMI, depression, anxiety, cynical hostility, optimism, positive affect, social participation and social integration) (OR 0.82, 95% CI 0.66 to 1.02).

    The researchers also divided perceived neighbourhood social cohesion into four categories: low, low-moderate, moderate-high and high. When age, gender, race, marital status, education and total wealth were adjusted for, people with high perceived neighbourhood social cohesion were at reduced risk of heart attack compared to people with low social cohesion. Again, this association was no longer significant if all confounders were adjusted for.

     

    How did the researchers interpret the results?

    The researchers concluded that “higher perceived neighbourhood social cohesion may have a protective effect against myocardial infarction”.

     

    Conclusion

    This US cohort study found that higher social cohesion was associated with a reduced risk of heart attack. However, the association became non-significant once the researchers adjusted for all behavioural (such as smoking or exercise), biological (such a BMI) and psychosocial (such as depression) factors that could act as potential confounders.

    It is difficult to draw any meaningful interpretation from these results. Perceived social cohesion in this study was only measured by asking people how much they agreed with four simple statements about whether they liked living in the area, whether people in the area were friendly and if they could be trusted. This tells us little about the sociodemographic structure of the area, or the individuals’ interpersonal relationships with others.

    Also, despite the large initial sample size, there were relatively few heart attacks over the four years. Heart attack cases were also noted by individual or proxy-self report, rather than a review of medical records, which may also have led to errors.

    There are a variety of biological, hereditary and lifestyle factors that are well known to be associated with greater risk of cardiovascular disease, and various other psychological ones that have been speculated (such as stress).

    As the results of this study suggest, it is likely that any link between risk of heart attack and perceived social cohesion is being influenced by a varied mix of other factors.

    If you want to try and reduce your risk of a heart attack, maintaining a healthy weight through diet and exercise, avoiding smoking and limiting alcohol intake are a great start. 

    Simply relying on your neighbours to cut your risk of heart attack is probably unwise.

    Analysis by Bazian. Edited by NHS ChoicesFollow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

    Links To The Headlines

    Having good neighbours can help cut heart attack risk, study shows. The Independent, August 18 2014

    Friendly neighbours could lower the risk of heart attack, study finds. The Daily Telegraph, August 18 2014

    Good neighbours can keep your heart healthy: Chance of a heart attack found to be a fifth lower if you live in a friendly area. Daily Mail, August 19 2014

    Links To Science

    Kim ES, Hawes AM, Smith J. Perceived neighbourhood social cohesion and myocardial infarction. Journal of Epidemiology and Community Health. Published online August 18 2014



  • Targeted brain stimulation 'could aid stroke recovery'

    "Stimulating the part of the brain which controls movement may improve recovery after a stroke," BBC News reports after researchers used lasers to stimulate a particular region of the brain with promising results in mice.

    The researchers were looking at a sub-type of stroke known as ischaemic stroke, where a blood clot blocks the supply of blood to part of the brain.

    With prompt treatment an ischaemic stroke is survivable, but even a temporary block to the blood supply can cause brain damage, which can impact on multiple functions such as movement, cognition and speech. Attempting to recover these functions is now an important aspect of post-stroke treatment.

    The researchers used a technique called optogenetics in this study. Optogenetics uses a combination of genetics and light, where genetic techniques are used to "make" (code) certain brain cells sensitive to the effects of light. Light is produced by a laser and delivered through an optical fibre.

    The researchers used light to stimulate an area of the brain (the primary motor cortex) in mice which had stroke-related brain damage. After stimulation, the mice's performance improved in behaviour tests assessing sensation and movement.

    But to use this technique in humans, brain cells would have to be made sensitive to light, possibly by introducing a gene coding for a light-sensitive channel into nerve cells using gene therapy techniques. It is unclear whether this would be feasible based on current technology and techniques.

     

    Where did the story come from?

    The study was carried out by researchers from Stanford University School of Medicine in the US.

    It was funded by the US National Institutes of Health, the National Institute of Neurological Disorders, a Stroke Grant, Russell and Elizabeth Siegelman, and Bernard and Ronni Lacroute.

    The study was published in the peer-reviewed journal PNAS.

    The research was well reported by BBC News.

     

    What kind of research was this?

    This animal study aimed to determine whether stimulating nerve cells in certain undamaged parts of the brain could help recovery in a mouse model of stroke.

    Animal research such as this is a useful first step in investigating whether treatments could potentially be developed for testing in humans.

     

    What did the research involve?

    The researchers used a mouse that had been genetically engineered so the nerve cells in the part of the brain responsible for movement (the primary motor cortex) produced an ion channel sensitive to light. When light is shone on the nerve cells expressing this ion channel, the ion channel opens and the nerve cell is activated.

    The researchers used healthy mice, as well as mice with brain damage caused by stopping blood flow in one of the arteries that supplies blood to the brain. This mimics the damage that occurs during an ischaemic stroke. The damage occurred in a different part of the brain from the primary motor cortex (the area that was stimulated). 

    The researchers looked at whether stimulating the nerve cells in the primary motor cortex using light from a laser could promote recovery in a mouse model of stroke. This combination of light and genetics is called optogenetics.

     

    What were the basic results?

    Light stimulation of the nerve cells in the undamaged primary motor cortex significantly improved brain blood flow, as well as blood flow in response to brain activity in "stroke mice". It also increased the expression of neurotrophins, a family of proteins that promotes the survival, development and function of nerve cells, and other growth factors.

    Stimulation of the nerve cells in the primary motor cortex also promoted functional recovery in the "stroke mice". "Stroke mice" who received stimulation showed faster weight gain and performed significantly better in a sensory-motor behaviour test (the rotating beam test).

    Interestingly, stimulations in normal "non-stroke mice" did not alter motor behaviour or expression of neurotrophins.

     

    How did the researchers interpret the results?

    The researchers concluded that, "These results demonstrate that selective stimulation of neurons can enhance multiple plasticity-associated [the brain's ability to change] mechanisms and promote recovery."

     

    Conclusion

    This mouse model of stroke has found that stimulating nerve cells in the part of the brain responsible for movement (the primary motor cortex) can lead to better blood flow and the expression of proteins that could promote recovery, as well as leading to functional recovery after stroke.

    But it remains to be determined whether a similar technique could be used in people who have had a stroke.

    The mice were genetically modified so nerve cells in the primary motor cortex produced an ion channel that could be activated by light. The nerve cells were then activated using a laser.

    To use this technique in humans, a gene coding for a light-sensitive channel would have to be introduced into nerve cells, possibly using gene therapy techniques.

    Gene therapy in people is very much in its infancy, so it is unclear whether this would be achievable, let alone safe. The last thing you would want to do with a brain recovering from stroke-related damage is to make that damage worse.

    Overall, this interesting technique shows promise, but much more research needs to be done before there will be any practical applications in the treatment of stroke patients.

    Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

    Links To The Headlines

    Brain stimulation 'helps in stroke'. BBC News, August 19 2014

    Links To Science

    Cheng MY, Wang EH, Woodson WJ, et al. Optogenetic neuronal stimulation promotes functional recovery after stroke. PNAS. Published online August 18 2014



  • Bone marrow drug could treat alopecia

    “Alopecia sufferers given new treatment hope with repurposed drug,” The Guardian reports.

    Alopecia is a type of autoimmune condition where the body’s own immune cells start to attack the hair follicles for an unknown reason, leading to hair loss.

    This new research actually involved two phases, one involving mice and one involving humans.

    The researchers identified the specific type of immune cell (CD8+NKG2D+ T cells) that is involved in this autoimmune process, and identified the signalling pathways that stimulate the activity of these cells.

    The researchers then demonstrated that using molecular treatments to block these signalling pathways was effective in preventing and reversing the disease process in mice genetically engineered to develop alopecia.

    These findings in mice were followed by promising results in three people with moderate to severe alopecia. These people were treated with ruxolitinib, which is currently licensed in the UK to treat certain bone marrow disorders. All three patients demonstrated “near-complete hair regrowth” after three to five months of treatment.

    This promising research is in very early stages. Ruxolitinib has been tested in only three people with alopecia, which is far too small a number to make any solid conclusions about the effectiveness or the safety of this treatment in people with alopecia.

    The safety and efficacy would need to be tested in many further studies involving larger numbers of people, and it would also need to be tested against other currently used treatments for alopecia, such as steroids.

     

    Where did the story come from?

    The study was carried out by researchers from Columbia University in New York. The study received various sources of financial support including US Public Health Service National Institutes of Health, the Columbia University Skin Disease Research Center, the Locks of Love Foundation and the Alopecia Areata Initiative.

    The study was published in the peer-reviewed scientific journal Nature Medicine.

    The media gives varied reports of this study. The Mail in particular is overly premature, as the current study is a very long way away in terms of research steps before knowing whether there could be a new “standard treatment for the condition”.

    Also, references to a “baldness pill” are potentially misleading as they could lead people to think that this treatment, or similar, would be effective against the most common type of baldness, male pattern baldness.

     

    What kind of research was this?

    This was a laboratory and mouse study that aimed to examine the cellular processes that cause alopecia and to try and investigate a treatment to reverse the process.

    Alopecia is a condition where body hair falls out, ranging from just a patch of hair on the head to the entire body hair. It is understood to be a type of autoimmune condition where the body’s own immune cells start to attack the hair follicles. Causes are not completely understood, with associations with stress and genetics speculated. Unfortunately, although various treatments may be tried (most commonly corticosteroids) there is currently no cure for alopecia.

    The autoimmune process is thought to be driven by T lymphocyte cells (a type of white blood cell). Previous laboratory studies in mouse and human models have shown that transfer of T cells can cause the disease. However, effective treatments are said to be limited by a lack of understanding of the key T cell inflammatory pathways in alopecia.

    The researchers had previously identified a particular subset of T cells (CD8+NKG2D+ T cells) surrounding hair follicles in alopecia, as well as identifying certain signalling molecules that seem to stimulate them. In this study, the researchers aimed to further investigate the role of these specific T cells using a group of mice genetically engineered to spontaneously develop alopecia, and also human skin samples.

     

    What did the research involve?

    First of all the researchers examined skin biopsies from genetically engineered mice that had developed alopecia to confirm that these specific CD8+NKG2D+ T cells were infiltrating the hair follicles. They confirmed that there was an increase in numbers of these specific T cells, increase in total number of cells, and also noticed that there was an increase in growth of lymph nodes in the skin. They found that the type of T cell infiltrating the skin and infiltrating the lymph nodes was the same. They examined the genetic profile of these T cells from the lymph nodes.

    They then looked into the role of these specific T cells in disease development by transferring these specific T cells, or overall cells from the lymph nodes, into thus far healthy genetically engineered mice that had not yet developed alopecia.

    This was in order to confirm that the CD8+NKG2D+ T cells were the dominant cell type involved in the development of the disease and were sufficient to cause the disease.

    The researchers then examined the gene activity in skin samples from the genetically engineered mice, and from humans with alopecia.

    They identified several genes that were overexpressed around the areas of alopecia, as well as several signalling molecules that are drivers of this abnormal T cell activity, including interleukins 2 and 15, and interferon gamma. 

    The researchers therefore then wanted to see whether using drug treatments that could block these signalling molecules would prevent disease development.

    To do this they grafted skin from mice that had developed alopecia on to the backs of mice who had not yet developed the condition. They then tested the effectiveness of drug treatments that can block the signalling molecules to see if they could prevent or reverse the disease.

    Finally, they followed their results in mice with tests in three people with alopecia.

     

    What were the basic results?

    When currently healthy mice were grafted with the skin of mice who had developed alopecia, 95-100% of them developed alopecia within 6 to 10 weeks. Giving antibodies to neutralise interferon gamma at the time of grafting prevented alopecia development. Giving antibodies to block interleukins 2 and 15 had a similar effect.

    However, though the researchers could prevent development if given at the same time, none were able to reverse the process if given after alopecia had developed.

    They then investigated whether they could block other signalling molecules that are involved in the downstream pathway from interferon gamma (called JAK proteins). Ruxolitinib (currently licensed in the UK to treat certain bone marrow disorders) is a molecule that blocks JAK1/2 proteins. Tofacitinib is another molecular treatment (not currently licensed for any condition in the UK) that blocks another (JAK3). When these two treatments were given at the same time the alopecia skin samples were grafted on to the healthy mice, the mice no longer developed alopecia.

    The researchers then tested whether giving tofacitinib seven weeks after grafting could reverse alopecia. Treatment did result in “substantial hair regrowth” all over the body and reduced numbers of T cells, which persisted for a few months after stopping treatment. They also tested whether these two JAK inhibitor treatments were effective when topically applied (rubbed into the skin on the back) instead of given by mouth, and found that they were, with hair regrowth occurring within 12 weeks.

    The human tests involved three people with moderate to severe alopecia who were given 20mg of ruxolitinib by mouth twice daily.

    All three people demonstrated “near-complete hair regrowth” within three to five months of treatment.

    No information on whether these people developed side effects was provided in the study.

     

    How did the researchers interpret the results?

    The researchers conclude that their results demonstrate that CD8+NKG2D+ T cells are the dominant cell type involved in the disease process of alopecia. They say that “the clinical response of a small number of patients with alopecia to treatment with the JAK1/2 inhibitor ruxolitinib suggests future clinical evaluation of this compound or other JAK protein inhibitors currently in clinical development is warranted”.

     

    Conclusion

    This is valuable laboratory research that identifies the specific type of immune cell (CD8+NKG2D+ T cells) that is involved in the disease process of alopecia. It further identifies several signalling molecules that are drivers of this T cell activity.

    The researchers then demonstrate that giving two molecular treatments to block the signalling molecules – ruxolitinib (currently licensed in the UK to treat certain bone marrow disorders) and tofacitinib (not currently licensed for any condition in the UK) – were effective in preventing and reversing the disease process in mice with alopecia.

    These findings in mice were followed by promising results in three people with moderate to severe alopecia who were treated with ruxolitinib. All three patients demonstrated “near-complete hair regrowth” after three to five months of ruxolitinib treatment.

    These are promising results into the study of potential treatments for this devastating autoimmune condition, which currently has no cure.

    However, it is important to realise that this research is in the very early stages. So far ruxolitinib treatment has been tested in only three people with alopecia, which is far too small a number to make any solid conclusions about the effectiveness or the safety of this treatment in people with alopecia. This drug is currently not licensed for use in this condition. It would need to go through many further clinical trial stages in larger numbers of people with alopecia. It would also need to be tested for safety and efficacy against other currently used treatments for alopecia, such as steroids.

    Overall there is some way to go before we could know whether ruxolitinib holds real promise as a treatment for alopecia.

    Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

    Links To The Headlines

    Alopecia sufferers given new treatment hope with repurposed drug. The Guardian, August 17 2014

    Pill that can cure baldness in five months: Twice-a-day tablet that allows alopecia sufferers’ hair to grow back set to become standard treatment for condition. Daily Mail, August 18 2014

    Baldness pill to cure alopecia. Metro, August 18 2014

    Links To Science

    Xing L, Dai Z, Jabbari A, et al. Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition. Nature Medicine. Published online August 17 2014



  • Depression 'common' in early Parkinson’s

    “Depression more common in early Parkinson’s,” BBC News reports, as a new study investigates the impact this degenerative condition can have on mental health.

    Parkinson’s disease is a neurological condition caused by a lack of the chemical dopamine in the brain. Alongside the characteristic movement symptoms such as involuntary shaking, mental health symptoms including depression, anxiety and dementia are relatively common in people with Parkinson’s.

    However, it is unclear whether these symptoms are directly caused by the disease process of Parkinson’s or whether there are other factors (for example, psychosocial) that may be involved in both.

    This study compared people with newly diagnosed Parkinson’s disease and healthy controls over two years to see if symptoms developed and changed.

    The researchers found that depression, fatigue, apathy and anxiety were more common at the time of diagnosis in people with Parkinson’s disease than healthy controls. Apathy and psychosis also increased over the two years in people with Parkinson’s.

    This study demonstrates how a variety of mental health problems can be common in early Parkinson’s disease, something patients need to be aware of.

    But we do not know whether these symptoms had newly developed as a direct result of the disease process, or whether these symptoms were present long before, or whether they even arose due to the “shock” of diagnosis.

    Read more advice about living with a long-term condition.

     

    Where did the story come from?

    The study was carried out by researchers from University Hospital Donostia, San Sebastián, Spain; Perelman School of Medicine at the University of Pennsylvania; and the Department of Veterans Affairs at Philadelphia VA Medical Center, US.

    Funding was provided by the Michael J. Fox Foundation for Parkinson’s Research and the following funding partners: Avid Radiopharmaceuticals, Abbott, Biogen Idec, Covance, Bristol-Myers Squibb, Meso Scale Discovery, Piramal, Eli Lilly and Co, F. Hoffman-La Roche Ltd, GE Healthcare, Genentech, GlaxoSmithKline, Merck and Co, Pfizer Inc, and UCB Pharma SA.

    The study was published in the peer reviewed medical journal, Neurology.

    BBC News’s reporting of the study was accurate and included some useful quotes from independent experts.

     

    What kind of research was this?

    This was a prospective cohort study that aimed to look at the course of mental health and cognition symptoms over two years in people with newly diagnosed Parkinson’s disease.

    Parkinson’s is a neurological condition caused by a lack of the chemical dopamine in the brain that affects the nerve cells. This causes characteristic symptoms including tremor, rigidity and slow movements. Mental health symptoms including dementia, depression, anxiety, and sometimes psychosis (such as hallucinations and delusions), have also long been associated with Parkinson’s.

    However, as the researchers say, it is unclear to what extent these “neuropsychiatric symptoms” are caused by the general degeneration of the nerve cells that occurs in Parkinson’s, or whether they could be caused by other psychosocial factors. Another possibility is that they could arise as side effects of the drugs often used to treat Parkinson’s.

    So looking at a newly diagnosed, untreated population of people with Parkinson’s and following them through the first two years of their condition should help to see how these mental health symptoms develop and progress. 

     

    What did the research involve?

    This research was called the Parkinson’s Progression Markers Initiative (PPMI) study, which was an international study conducted in 16 US and five European sites. The study enrolled 423 people with newly diagnosed Parkinson’s disease, who met diagnostic criteria for the condition, had not yet received any treatment and were currently free from dementia. As a comparison group they enrolled 196 healthy controls without the condition.

    A subset of people with Parkinson’s and healthy controls were assessed at baseline, 12-month and 24-month follow-up. People with Parkinson’s only had also been assessed at six months.

    The assessments at baseline and each follow-up point included:

    • depression on the Geriatric Depression Scale
    • cognitive ability on the Montreal Cognitive Assessment (MoCA)
    • impulsive behaviour (compulsive or repetitive behaviours due to poor control, such as gambling, sexual, eating, excessive wandering) on the Questionnaire for Impulsive-Compulsive Disorders in Parkinson’s Disease
    • excessive daytime sleepiness on the Epworth Sleepiness Scale and other sleep disorders on the REM sleep behaviour disorder screening questionnaire
    • movement disorders and other aspects of disease severity on the Movement Disorders Society Unified Parkinson’s Disease Rating Scale
    • anxiety on the State-Trait Anxiety Inventory
    • sense of smell on the University of Pennsylvania Smell Identification Test

    People with Parkinson’s could start treatment with dopamine replacement therapy (often levodopa) at any time after diagnosis. Dopamine replacement therapy is designed to help improve symptoms, though side effects can be wide ranging.

    They were considered to have received treatment if they had been prescribed it for at least one year, and were still prescribed the treatment at the end of the study (the two-year follow-up). Treatment had been started by 9.6% of patients with Parkinson’s disease at six months, by 58.8% at 12 months and 81.1% at 24 months.

    Comparisons were made between the Parkinson’s and control groups.

     

    What were the basic results?

    Overall, people with Parkinson’s had significantly more symptoms of depression, anxiety, fatigue and apathy at all time points compared to controls, and symptoms of apathy and psychosis increased over time in the people with Parkinson’s.

    Depression

    At enrolment 13.9% of people with Parkinson’s disease and 6.6% of healthy controls screened positive for depression on the GDS.

    There was a non-significant increase to 18.7% of people with Parkinson’s disease having depression at 24 months, compared to a decrease to 2.4% in the health control group. The proportion of people with Parkinson’s disease taking an antidepressant increased from 16% at baseline to 25% at 24 months.

    Cognition

    The average MoCA score of people with Parkinson’s disease decreased significantly from 27.1 at baseline to 26.2 at month 24. The cutoff for mild cognitive impairment is below 26. Using this cutoff, 21.5% of people with Parkinson’s disease were cognitively impaired at baseline, 34.2% at 12 months, and 35.5% at 24 months. Mean scores in the health control group also decreased overtime from 28.5 at baseline to 27.7 at 24 months.

    Other neuropsychiatric symptoms

    The proportion of people with Parkinson’s disease with positive scores on the Movement Disorders Society Unified Parkinson’s Disease Rating Scale for fatigue and apathy at baseline was 50% and 16.7%, respectively, increasing to 61.5% and 30.2% at 24 months. These proportions were significantly higher than the health control group at all timepoints. Similarly, anxiety symptoms were significantly higher in the Parkinson’s disease than health control group at all timepoints, though anxiety scores did not increase over time in the Parkinson’s disease group. The prevalence of psychosis symptoms increased in the Parkinson’s disease group from only 3.0% of people at baseline, to 5.3% at 12 months and 10% at 24 months.

    The proportion of people with Parkinson’s disease with impulsive behaviour symptoms was 21% at baseline and did not significantly increase during follow-up; nor was there a significant difference between Parkinson’s disease and health controls at any time point. There was a trend for daytime sleepiness symptoms to increase in people with Parkinson’s disease, but again no significant difference was seen compared with health controls.

    Relation to treatment

    At 24 months, 81% of people with Parkinson’s disease had started dopamine replacement therapy, and 43.7% had been taking it for at least one year. This group reported significantly more new problems with impulse control and excessive daytime sleepiness compared to baseline.

     

    How did the researchers interpret the results?

    The researchers conclude that multiple neuropsychiatric problems are more common in newly diagnosed, untreated people with Parkinson’s compared with the general healthy population. These problems tend to remain relatively stable in early disease, while cognition slightly deteriorates. Starting dopamine replacement treatment is associated with increasing frequency of several other neuropsychiatric problems.

     

    Conclusion

    This cohort study benefits from its prospective design, following a group of people newly diagnosed with Parkinson’s disease across the course of two years compared to a group of healthy controls. It also benefits from being an international, multicentre study including a fairly large sample size, and from conducting regular symptom assessments using a series of validated tools.

    However, there was quite a high loss to follow-up. From 423 people with Parkinson’s assessed at study start, 62% were available for 12 month follow-up, and only 23% at 24 months. This is an important limitation that may affect the reliability of the results.

    The study demonstrates that people with Parkinson’s already at the time of diagnosis seemed to have higher symptoms of depression, anxiety, fatigue and apathy than the healthy controls. The proportion of people with Parkinson’s who had fatigue and apathy increased over the two years. Also the proportion with symptoms of psychosis, though low, did increase throughout the study.

    Cognitive ability deteriorated significantly over the two years of the study in people with Parkinson’s disease.

    The use of dopamine replacement treatment was associated with the development of new symptoms of impulse control and excessive daytime sleepiness. However, these results were based on a small sample.

    Therefore, the study provides us with an indication that certain mental health symptoms of depression, anxiety, fatigue and apathy may already be present at the time that Parkinson’s is first diagnosed.

    This suggests that these symptoms are not likely to be caused by Parkinson’s treatment, as the people hadn’t started treatment yet, but it can’t really tell us much more about how they developed.

    It seems possible that they may be caused by the general nerve degeneration process that happens in the development of Parkinson’s. However, we don’t know whether these symptoms may have been present long before the person developed Parkinson’s (such as whether the person had a lifetime history of depression and anxiety problems). Therefore, we don’t know overall whether they are caused by the Parkinson’s disease process.

    It could be the case that there are other genetic, health psychosocial or lifestyle factors involved in the relationship that may put the person at risk of both these mental health conditions and Parkinson’s.

    This study is a valuable contribution to the research into Parkinson’s disease and its associated mental health symptoms. But unfortunately it provides no solid answer to the direct cause of development all of these symptoms.

    Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

    Links To The Headlines

    Depression 'more common' in early Parkinson's. BBC News, August 16 2014

    Links To Science

    de la Riva P, Smith K, Xie SX, et al. Course of psychiatric symptoms and global cognition in early Parkinson disease. Neurology. Published online August 15 2014



  • Macmillan finds cancer survival 'postcode lottery'

    “Cancer postcode lottery ‘costs 6,000 lives a year’,” reports The Times.

    This, and similar headlines, are based on cancer survival figures compiled by Macmillan Cancer Support. The cancer charity’s report suggests that the proportion of people who die within a year of a cancer diagnosis is two-thirds higher in poor-performing areas, compared with high-performing areas.

    These are shocking statistics, but it’s important to bear in mind that one-year cancer survival rates don’t give us the whole picture about the state of cancer care in England.

    In a press release, MacMillan reports that around 6,000 more people could survive for at least 12 months after their cancer diagnosis if average survival across the whole of England matched the top 10% of local healthcare regions.

    It identified areas such as Telford, Medway and Dagenham as having among the lowest cancer survival rates. Leafy Surrey, Dorset and Richmond had among the best cancer survival rates, according to the charity.

    MacMillan suggests that the differences in survival could be explained by differences in waiting times for urgent referrals and start of treatment, which should be a set standard across the country. The charity calls for this “looming crisis” in cancer care to be addressed.

     

    What does the MacMillan cancer survival report say?

    MacMillan used data from the Office for National Statistics (ONS) and London School of Hygiene and Tropical Medicine to find the estimates for one-year survival for all types of cancer combined for all adults (aged 15 to 99) in 2011.

    The average one-year survival for the whole of England was 68%. This means that roughly two-thirds of all people in England diagnosed with cancer survived for 12 months after they were diagnosed, and a third of people died by 12 months. In the 10% of regions with the best one-year survival rates in the UK, one-year survival was almost three-quarters, at 71%.

     

    What is the reason for the differences in one-year cancer survival?

    Links To The Headlines

    Cancer patients: best and worst places to live for survival revealed. The Daily Telegraph, August 15 2014

    Postcode lottery 'is killing 6,000 cancer patients every year': Proportion who die within year of diagnosis is two-thirds higher in worst-performing areas than the best. Mail Online, August 15 2014

    Cancer treatment in England: 'Inexcusable postcode lottery' causes 6,000 'needless' deaths. Daily Express, August 15 2014