Category Archives: Neurology

Are compliments a part of your day-to-day life? (Getty Images) (Getty Images)

Did you know that giving and receiving compliments, when done regularly, does far more for our overall wellbeing than just providing some quick flattery?

Engaging in these acts of kindness on a regular basis (following World Kindness Day which fell earlier this week), really is worth it for the very real neurological impact it has on our brains and us.

That said, one in 10 Brits have never given or received a compliment, according to a new study something that needs to change (when done genuinely, of course).

And looking at the UK, when 1,5000 British adults were asked where is home to the most kind and complementary people, the majority vote (10%) said London. This may come as a surprise for those who believe 'it's much friendlier up north'...

Though Liverpool and Manchester did come in second place, and Newcastle third.

Here, Dr Ritika Suk Birah, HCPC accredited consultant counselling psychologist sheds some light on what actually goes on in our brains when exchanging compliments.

The most common emotions associated with well-intentioned compliments are happiness (43%), confidence (22%) and pride (21%), according to the study. Although in true British fashion, 20% of us do feel somewhat awkward, 17% feel embarrassed and 5% of Brits panic in the face of a compliment.

But while there's definitely a time and place for compliments, for those that are sincere and kind, it's probably worth us getting over any awkwardness to reap the benefits.

"When we smile and compliment each other it can have several beneficial effects on our self-esteem and overall wellbeing. Compliments serve as external validation reaffirming our sense of self-worth and competence," says the psychologist, enlisted by ScS, which conducted the survey.

"We can use neuroscience to understand that compliments ignite brain regions associated with reward and positive self-perception, such as the striatum and medial prefrontal cortex."

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"These neural activities trigger the release of endorphins and serotonin, two neurotransmitters known for their role in fostering feelings of joy, contentment and emotional wellbeing."

And whether you're the one dishing them out, or flattered by one you've received, the benefits work both ways.

"Receiving compliments can create a psychological positive feedback loop. When we feel good about ourselves, we are more likely to engage in positive behaviours, such as setting and achieving goals, which, in turn, reinforces our self-esteem," explains Dr Suk Birah.

"The act of giving compliments constructs a culture of mutual appreciation and respect, we strengthen social bonds and nurture positive interpersonal relationships."

Of course, we shouldn't need compliments all the time just to like ourselves, but they can certainly come as a welcome addition. "Compliments have transformative power in creating happiness, improving our overall sense of wellbeing which can lead to a more positive and emotionally fulfilling social environment," says Dr Suk Birah.

What was the last compliment you received or gave to someone else?

Read more: Half of women believe theyre just entering their 'confidence era'

Continued here:
Psychologist reveals the neurological impact of giving and receiving compliments - Yahoo Lifestyle UK

There has never been a more exciting time in Alzheimer care than today. Promising innovations in therapies and diagnostics for this most common form of dementia are emerging at a faster pace than at any other time in medicine. At the same time, science is revealing that, for some, preventive behavioral measures can meaningfully delay progression. These developments together provide greater reason for optimism for those at risk of Alzheimer than at any other time in recent memory.

And these medical achievements couldnt come at a better time. More than 6 million patients nationwide live with Alzheimer disease (AD). By 2050, this number could reach nearly 13 million with costs of care topping $1 trillion.1

Yet, this rapid pace of change also threatens to confuse providers and patients who may not be up to date on the latest science on Alzheimer. Dispelling long-perpetuated misunderstandings of this complicated condition may open more avenues leading to better outcomes.

#1: Only older patients need to worry about AD.

#2: AD is primarily an inherited genetic disease.

#3: Most patients dont want to know if they are at risk of developing AD.

#4: Only high-powered imaging tests can help evaluate for AD.

#5: Only pharmacological therapies can meaningfully address AD.

Fact: AD often begins in the brain in middle age sometimes decades before symptoms emerge. While age increases risk, it is not a direct cause of Alzheimer and patients of all ages can begin to take steps to potentially slow cognitive decline. A recent study conducted by the CDC showed pediatric patients can reduce their risk of developing AD later in life in a number of ways, from managing their blood pressure and blood sugar, to being physically active.2

Fact: Genetics are only one possible factor in the development of AD, and having a family history of Alzheimer does not necessarily doom one to developing the disease. At the same time, a lack of family history does not eliminate the possibility a person will develop Alzheimer. There are 2 categories of genes that influence whether a person develops a disease: risk genes and deterministic genes. While Alzheimer genes have been found in both categories, less than 1% of AD cases are believed to be because of deterministic genes.3

Even those who have these genes may never develop AD; risk genes increase the likelihood of developing a disease, but do not guarantee it will happen. Researchers have found several such genes that increase risk. Apolipoprotein (APOE) 4, one common form of the APOE gene, has shown to have the strongest impact on risk, as researchers estimate that between 40-65% of people diagnosed with Alzheimer have the APOE-e4 gene.3 Those who inherit copies of APOE-e4 from their parents have an increased risk of developing AD, but it is not a certainty. These individuals can still take steps to mitigate their risk by reducing environmental factors or taking preventative steps to better their condition.

Fact: A recent Harris Poll commissioned by Quest Diagnostics found that only 4 in 10 Americans surveyed said they would speak to their clinician right away if experiencing memory or cognitive loss, suggesting an aversion to being diagnosed with a dementia like Alzheimer. Yet, when asked directly, the majority (7 out of 10) expressed a desire to know if they have AD as early as possible to allow for treatment illustrating a willingness to confront the prospect of a scary medical diagnosis if treatment can enhance the odds of a favorable outcome.4

Fact: New diagnostics, including those using simple blood tests, are rapidly opening doors to accessible risk evaluation for many. These blood tests generally help assess -amyloid or tau, 2 brain proteins associated with Alzheimer pathology in the brain. Amyloid- creates plaques which may lead to tangles of tau in the brain. For this reason, many diagnostic companies, including Quest Diagnostics, are focused largely on tests for amyloid protein, given its potential to detect early stages of disease.5

Growing acceptance of blood tests is needed, as emerging pharmaceutical treatments for Alzheimer will require better tools to assess patients. This is because conventional tests, such as PET scans and those that use cerebral spinal fluid, are expensive and specialist dependent. Plus, there is a growing shortage of neurologists.6 Laboratory tests, when combined with other screening methods, can be a powerful tool in crafting an effective patient care plan in fact, in a survey of physicians, 84% said testing for early risk of AD will lead to earlier and improved disease management. Among U.S. adults, 86% agree, stating they believe blood tests for the early detection of Alzheimer risk will increasingly become a regular part of preventative care.7

Fact: For some, Alzheimer may be a preventive condition. New research shows it is possible to reduce risk of AD or at least slow progression. Some studies suggest people who exercise more, including walking an increased number of steps at an advanced pace, have better memory retention and are less likely to develop conditions like Alzheimer or dementia.8 Studies have also shown creative activities like playing games, learning an instrument or reading books may help preserve brain function.9 As a patient gets older, it can be more challenging to maintain social activity, though some research shows this can also help preserve mental function and slow mental decline.10 Yet, the same lifestyle choices and behaviors that can reduce risk of developing heart disease, diabetes and other chronic conditions may also offer some protection against Alzheimer. Addressing depression and hearing loss are other key steps to reduce risk.11

Fact: Cognitive decline is often not because of dementia and can be reversed. There are other potentially reversible causes of cognitive decline that can mimic dementia. These include things as minor as medication side effects or hormonal imbalances, and can be as severe as other chronic conditions like HIV. In 1 study, as many as one in 5 (19.17%) individuals (most over the age of 60 years) with cognitive issues were found to have a reversible condition, such as adverse effects from medication or hormone imbalances.12 Without screenings, conditions that mimic dementia may go undiagnosed in a patient and cause adverse health effects. If properly diagnosed, these conditions, may be treated to potentially slow or reverse any associated cognitive decline.13

Certain tools aim to address this. As an example, uMETHOD Health, a health technology company specializing in precision medicine for chronic diseases, recently worked with Quest Diagnostics to nationally debut a risk assessment and care plan service for patients with cognitive decline. The service, called RestoreU, employs artificial intelligence to crunch data on a persons lab test results and health history, including comorbidities, lifestyle habits and medications, to help identify if risk of cognitive decline is because of a reversible cause.14

With so much attention on emerging therapies for AD, it is easy to overlook the growing body of science suggesting a preventive care approach can help delay the onset of Alzheimer and other dementias in some patients. When it comes to conditions like Alzheimer and dementia, one thing remains clear: patients and providers both seek the ability to provide an early diagnosis and craft the best care plan possible. Though so many remain affected by cognitive conditions, there are steps that can be taken, as with any other health condition, to mitigate risk and ease symptoms. By speaking with a provider about these changes, patients may find these conditions more manageable than first anticipated.

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Alzheimer Disease: Separating Fact from Fiction - Neurology Live

WEDNESDAY, Nov. 15, 2023 (HealthDay News) -- Cardiac 18F-dopamine positron emission tomography (PET) can identify at-risk individuals who are subsequently diagnosed with a central Lewy body disease (LBD), according to a study published online Oct. 26 in the Journal of Clinical Investigation.

David S. Goldstein, M.D., Ph.D., from the National Institutes of Health in Bethesda, Maryland, and colleagues assessed the predictive value of low versus normal cardiac 18F-dopamine PET in at-risk individuals. Thirty-four participants with three or more confirmed risk factors underwent serial cardiac 18F-dopamine PET at intervals of 1.5 years for 7.5 years or until diagnosis of Parkinson disease.

Nine and 25 patients had low and normal initial myocardial 18F-dopamine-derived radioactivity, respectively. The researchers found that eight of nine with low initial radioactivity and one of 11 with normal radioactivity were diagnosed with a central LBD (LBD+) at seven years of follow-up. All nine LBD+ participants had low 18F-dopamine-derived radioactivity before or at the time of diagnosis of a central LBD, while only one of the 25 participants without a central LBD had persistently low radioactivity.

"We think that in many cases of Parkinson and dementia with Lewy bodies the disease processes don't actually begin in the brain. Through autonomic abnormalities the processes eventually make their way to the brain," Goldstein said in a statement. "The loss of norepinephrine in the heart predicts and precedes the loss of dopamine in the brain in Lewy body diseases."

Abstract/Full Text

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Cardiac 18F-Dopamine PET: A Promising Predictor of Lewy Body ... - HealthDay

Months after the FDA approved valbenazine (Ingrezza; Neurocrine Biosciences) for the treatment of chorea associated with Huntington disease (HD), new interim data from the open-label extension (OLE) of the phase 3 KINECT-HD2 study (NCT04400331) continued to highlight the therapys longterm efficacy and safety. All told, improvements in chorea were observed at the first evaluation (week 2) when participants were taking the lowest dose of 40 mg, with efficacy sustained through week 50 at a maximal dose of 80 mg.1,2

After the completion of the phase 3 KINECT-HD study, adults with genetically confirmed motor-manifest HD entered the OLE where they received once-daily valbenazine starting at 40 mg for up to 156 weeks. In addition to safety evaluations, efficacy outcomes included change in Unified Huntingtons Disease Rating Scale Total Maximal (TMC) score, Clinical Global Impression of Change (CGI-C), and Patient Global Impression of Change (PGI-C). The data, which included outcomes up to week 50, were presented at the 30th Annual Meeting of the Huntington Study Group, held November 2-4, in Phoenix, Arizona.

Of 127 participants at the time of the analysis, 98 were from KINECT-HD. All told, mean TMC score reductions were observed by week 2 with valbenazine 40 mg (n = 118; 3.4 [3.1]) and sustained with maximal doses of 80 mg from week 8 (n = 110; 5.6 [3.6]) to week 50 (n = 66; 5.8 [4.1]). At week 50, 76.9% (50 of 65) of participants were CGI-C responders and 74.2% (49 of 66) were PGI-C responders. Among 125 patients who received treatment, 95.2% (n = 119) reported at least 1 treatment-emergent adverse event (TEAE) and 13.6% (n = 17) discontinued because of a TEAE. Falls (30.4%), fatigue (24.0%), and somnolence (24.0%) were among the most common TEAEs reported.

"These interim data provide insight on the clinically meaningful and sustained improvements participants are experiencing with INGREZZA for the treatment of chorea," Eiry W. Roberts, MD, chief medical officer at Neurocrine Biosciences, said in a statement. We look forward to analyzing additional data as they become available."

READ MORE: Patient Dosing Commenced in Phase 2 ASCEND Study of Parkinson Agent CVN424

Neurocrine also presented new substudy data from KINECT-HD using a wearable movement sensor, the first such study of its kind. Using the BioStamp nPoint system, participants wore 3 sensors (chest and anterior thighs) for 2, 7-day periods during the screening period and following the week 10 visit. A total of 27 patients (valbenazine: n = 12; placebo: n = 15) who wore the sensors for at least 5 hrs/day for at least 5 days during baseline and maintenance were included in the analysis. Results showed significant improvements in truncal chorea and gait asymmetry measures in the valbenazine (all P <.05) but not in the placebo group. Of note, 6 participants reported any sensor-related AE, all of which were mild.3

Valbenazine, a selective vesicular monoamine transporter 2 inhibitor, became the first such inhibitor FDA-approved for the treatment of chorea associated with HD in August 2023 based on results from the phase 3 KINECT-HD study and its OLE, KINECT-HD2. Similar in design, each study featured adults aged 18 to 75 years who had been diagnosed with either manifest HD or motor manifest HD who have sufficient chorea symptoms. In KINECT-HD, the agent met its primary end point, demonstrating a statistically significant placebo-adjusted reduction in Total Maximal Chorea (TMC) score of 3.2 units (P<.00001) from baseline to weeks 10 and 12.4

Read more from the original source:
Huntington Therapy Valbenazine Demonstrates Significant, Long ... - Neurology Live

Bruce Hughes, MD: Switching a little bit on this, I think its also incumbent upon us to not just talk about disease-modifying therapy and cognitive functioning, but we do know that physicality and physical exercise ties into mental health [treatment]. If the patients mental health is out of order, their physical health is never going to be maximally in order, so treating the whole patient is important. And then identifying what youre talking about, because I think we focus more here on cognition, but kind of tying in with that is fatigue, which is so hard to identify. Educating patients on cognitive tips is very important as far as not just your disease-modifying therapy, but things that you that help minimize the effects of the cognitive decline on your health.

Robert Naismith, MD: I agree. I think your mental health plays a huge role in the disease. We see this all the time when people are under stress, when people arent able to take care of themselves, they present with worsening. Thats something you really need to dig into and assess, and we see that all the time where people are trying to juggle parents who are not doing well and who are sick, and thats putting stress on the family or family dynamics between the spouse and is not the best, and this affects the disease. So I think what you brought up with exercise is an important thing that we talk about at every visit. Doing physical therapy as a tool to show you how to do stuff for yourself at home and then doing another visit to make modifications based upon the things that youve achieved with those exercises and really stressing [that] this is something thats going to help you do better, addressing mood. People have a lot of depression [and] anxiety, [and] sleep is an issue for a lot of people. This impacts how they feel and how the disease manifests itself in the fatigue, so we use a lot of antidepressants in practice. But not everybody feels like thats going to be the best thing for them, so we also have options for counseling. We have a list of counselors. One of the nice things is [that] people are now able to do counseling by , so they dont necessarily have to go to a place to do it, so a lot of my patients choose to pick a counselor in their area. They might do some in-person visits, they might do some [telehealth] visits, so I think the access is very good for that. But thinking about the whole patient in terms of their mood, their sleep, their comorbidities, exercise program, how theyre interacting with everybody, and if theres anything within your power to help that or get them to the professional that can help them do it together with you, those are the things that Im looking for my practice. As a multidisciplinary MS [multiple sclerosis] center I want to have the tools to say, well, this isnt my expertise, but I know someone who can help you with this; we need help to treat you in every way we can.

Bruce Hughes, MD: I think thats spot-on. The referral to mental health providers is big in multiple sclerosis management because unlike many patients, MS patients tend to have very good insight into their disease process, and to me, those are the ones who do the best with cognitive therapy and counseling. At your center, do you find much benefit in referrals to speech language cognitive therapy for ongoing assessment like what you would do with physical therapy or occupational therapy, or have you not found that quite as helpful?

Robert Naismith, MD: I think it depends upon the person, but we do make the recommendation when we have the referral for neurocognitive testing, thats going to be like a 2 or 2.5-hour battery where they can go through all the different domains of executive functioning, word finding, short-term memory, reading. Theyll go through all the different domains, and theyll check their baseline level so theyre able to get a real sense of their cognitive function, and also their mood. They also check for mood disorders as well. And then well have the specialist who does the testing explain everything to the patient and document and make a report. And then well also make a referral to speech cognitive therapy so that they can use those results and gain more insight and come up with strategies to adapt to them. It may also include a referral to vocational rehab if its going to affect their work issues and if the combinations need to be made so that theyre able to perform at their best. So it depends on the person, but we always offer with that neurocognitive referral a chance to see a speech cognitive therapist and also, if they are working, vocational rehab to try to make the accommodations that are going to help them be successful in the work setting.

Bruce Hughes, MD: I think that point is very good in that sometimes were identifying [whether it is] brain volume loss in the disease process or are there confounding variables on their cognitive functioning such as depression, such as sleep disturbance, which I think is huge and really underrecognized in the multiple sclerosis population. We should be doing a lot more assessment of sleep for whatever the cause of why theyre having sleep disturbance. Its just remarkably common. How do we how do we address and improve that?

Transcript is AI-generated and edited for clarity and readability.

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Improving Cognitive Awareness of Patients and Caregivers in MS ... - Neurology Live

Bruce Hughes, MD: When we were looking at the different therapies, I was looking at all of the high-efficacy therapies out there and the data on [the impact of] brain volume loss. It is striking how, when you look at it, it kind of boils down to 3 areas, and that is anti-CD20, S1P receptor modulators, and natalizumab with regard to best data on impacting the decrease in cerebral brain volume loss. That ties in with our high-efficacy [therapy], and utilizing that information, you can then, [in]s your discussionwith patients, come up with the best therapy that we think is optimal for them. I always bring up that we dont necessarily knock it out of the park with our first attempt, but what well do, the promise is not that well have an optimal outcome, but that well monitor and, if were not headed toward optimal outcome, well make a switch and well make an adjustment. Just based on that mantra of efficacy, tolerability, safety triad that needs to come together. Are there any other thingsthat we havent touched on that would be beneficial with regard to health care providers who are managing patients with multiple sclerosis?

Robert Naismith, MD: Just to recap, what weve been discussing is that you really need to shut down the acute inflammation as early as possible. You need to stop that process because, although its not perfectly correlated to chronic inflammation and neurodegeneration, there is definitely an input from acute inflammation of those processes. So stopping that acute inflammatory component is going to benefit the patient long term because nowadays we talk about expanding lesions and microglial activation, but what if we can prevent that in the first place? I feel like using these highly effective therapies to shut down the inflammatory reaction, the bloodstream break down early is going to benefit patients. Now, unfortunately, we probably dont catch patients at the very start of their disease. Were lucky with MS compared to other degenerative disorders that we do catch them quite early in the whole process, but they may have had MS for years before you even see them the first time. If you think maybe Epstein-Barr virus [EBV] is the spark that lights the fuse and they get EBV in their teens, like at the age of 17 [or] 18, there may be processes taking place with MS pathogenesis and the susceptible patient for many years before they present in their 20s, 30s, and 40s. We cant go back and reverse that, but what we can do is try to stop that inflammation and to slow down the processes that will take place from then on out.

We cant go back and stop the processes that have already taken place because we know that they already have the cognitive issues when they present. They already have changes in brain volume when they present with RIS [radiologically isolated syndrome] or their first episode. So you cant go back to the very, very beginning, but were still able to catch most patients quite early and get them on therapies. And I monitor them to make sure that were doing our best to stop the inflammation, stop new MRI lesions, and to do our best to stabilize the disease process and their symptoms.

Bruce Hughes, MD: Yes, I think that is right. Capturing the disease process before the horse is out of the barn. We talk a lot about this need for being able to impact the disease process centrally in the brain and spinal cord vs peripherally with our agents that shut down inflammation, so extremely well. But could you obviate the need for essentially acting if you treat the disease process early enough and effectively enough? To your point, we know this, right? Clinically isolated syndrome [CIS], the cognitive testing, just that theres the program, and I completely agree with that, is that you do neurocognitive testing on patients with CIS and theyre decidedly more defective than the general age-matched population. Likewise, and Ive always found this very interesting when were looking at this data for brain volume loss, we again have learned, whereas previously we thought that was a later manifestation of multiple sclerosis, that actually the brain volume loss, the speed with which the loss occurs, is most rapid in the first few years of diagnosis, not when its decades old. So I think that does encapsulate very well the importance. I think we tied in high-efficacy therapy, brain volume loss, cognitive functioning, and some tools to monitor and to help manage that in our MS patients.

Id like to thank you for sharing your expertise, Dr Naismith. Thank you for watching this Neurology Live Peers & Perspectives. If you enjoyed the content, please subscribe for our e-newsletters to receive upcoming Peers & Perspectives and other great content right in your inbox.

Transcript is AI-generated and edited for clarity and readability.

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Therapy Adjustments for Optimal, Early Intervention to Prevent ... - Neurology Live