Depression and Anxiety Linked to Accelerated Biological Aging in Adults

It is your doctor's responsibility to prevent depression and anxiety post stroke by having 100% recovery protocols.  If your doctors are having to treat depression and anxiety post stroke,  they are COMPLETE FUCKING FAILURES!

Depression and Anxiety Linked to Accelerated Biological Aging in Adults

Summary: Adults with advanced biological age are at a higher risk of depression and anxiety, according to a study that found participants with older biological age were 6% more likely to develop these mental health conditions at the 8.7-year follow-up compared to those who tested younger biologically.

Source: Columbia University

A study just released by Columbia Mailman School of Public Health and Peking University School of Public Health provides some of the first, large-scale evidence that processes of biological aging may contribute to risk of depression and anxiety.

Until now nearly all work to date had focused on poor mental health as a risk factor for accelerated aging. A complementary, but less-studied hypothesis is that the reverse process may also occur and accelerated processes of biological aging may, themselves, pose risks to depression/anxiety disorders of older adults.

The results are published online in Nature Communications.

The researchers tested associations of blood-chemistry measures of biological aging with prevalent and incident depression and anxiety among a half-million midlife and older adults in the UK Biobank, an ongoing study with 502,536 participants recruited in 2006–2010 at the age of 37–73 years with multiple follow-ups.

The findings showed that adults with more advanced biological age were more likely to experience depression and anxiety at baseline and were at higher risk of depression/anxiety over eight years of follow-up, as compared with peers who were the same chronological age, but who were tested to be biologically younger.

At the 8.7 year-follow up mark, participants with older biological age were at a 6 percent increased risk of incident depression and anxiety.

“Among older adults who were free of depression/anxiety at baseline, those whose blood indicated that they were biologically older than their chronological age would predict were more likely to develop depression or anxiety over follow-up compared with those whose blood indicated that they were biologically younger,” said Xu Gao, Ph.D., assistant professor at Department of Occupational and Environmental Health Sciences, School of Public Health, Peking University, China, and first author.

Depression and anxiety are common mental disorders that often co-occur and are associated with increased disability and mortality, especially in older adults. Prevention of depression and anxiety in older adults therefore has potential to mitigate disease burden in an aging population.

“This study helps confirm that identifying risk factors and mechanisms of vulnerability to mental disorders must be a public health priority, “observed Gao, who had been affiliated with the Columbia Mailman School Department of Environmental Health Sciences.

The research team had released two earlier papers regarding the connections of air pollution with biological aging (Aging Cell 2022) and with mental health (Environmental Health Perspectives 2023), respectively. “These findings complete the logical circle, demonstrating that air pollution may trigger depression/anxiety by accelerating biological aging,” said Gao.

The researchers analyzed the UK Biobank data for three overlapping groups of participants with whom Gao and corresponding senior author Daniel Belsky, Ph.D., associate professor of epidemiology at Columbia Mailman School of Public Health, followed up to provide information on their lifestyle and health, and provide biological samples.

The first group included all individuals providing baseline blood chemistry data required for calculation of biological age measurements and who completed mental health surveys at enrollment baseline (N = 424,299). The second group consisted of the subset of the first group who did not have prevalent depression/anxiety at baseline (N = 369,745).

The third group was the subset of individuals who did not have prevalent depression/anxiety at baseline and who also participated in the online follow-up mental health survey, a subset of 124,976 which helped inform the prospective associations between baseline biological aging and the syndromes of depression.

The findings showed that adults with more advanced biological age were more likely to experience depression and anxiety at baseline and were at higher risk of depression/anxiety over eight years of follow-up, as compared with peers who were the same chronological age, but who were tested to be biologically younger. Image is in the public domain

People with incident depression/anxiety experienced higher incidence of chronic conditions over follow-up as compared to those who did not have incident depression/anxiety (for diabetes, 6 percent vs. 3 percent; for cardiovascular diseases, 12 percent vs. 6 percent; and for cancers, 11 percent vs. 8 percent.

The research team notes that while the findings help establish a prospective link connecting older biological age with incident depression/anxiety, they do not address the mechanisms mediating this link, which could be formed at multiple stages in the progression of aging processes.

“We all age at the same rate in chronological terms. But from a biological perspective, some of us age faster than others, developing chronic disease and disability much earlier and living shorter, sicker lives,” said Belsky, who is also a member of the Butler Columbia Aging Center at Columbia University.

“We now have measurement tools that can quantify differences between chronological and biological age. In this study, we used two of these measurement tools to study the connection between aging and mental health.

“Findings suggest future directions for depression/anxiety risk assessment in older adults as well as the potential for therapies that target the biology of aging to contribute to the prevention of later-life depression/anxiety.”

About this depression and aging research news

Author: Press Office
Source: Columbia University
Contact: Press Office – Columbia University
Image: The image is in the public domain

Original Research: Open access.
“Accelerated biological aging and risk of depression and anxiety: evidence from 424,299 UK Biobank participants” by Xu Gao et al. Nature Communications

Potential Predictors of Motor and Functional Outcomes After Distributed Constraint-Induced Therapy for Patients With Stroke

Am glad my therapists never tried this on me. It would have been easy to tell this wouldn't work, just look at all the dead motor and pre-motor cortex areas. No signals were being generated from there. Which is the same reason non-use is wrongly applied most of the time to survivors.

 I would have had zero quality of life if I had to do CIT; no eating, no dressing, no bathroom, either 1 or 2.

Potential Predictors of Motor and Functional Outcomes After Distributed Constraint-Induced Therapy for Patients With Stroke

2008, Neurorehabilitation and Neural Repair

 
336
Potential Predictors of Motor and Functional Outcomes After Distributed Constraint-Induced Therapy for Patients With Stroke
Keh-chung Lin, ScD, OTR, Yan-hua Huang, PhD, OTR, Yu-wei Hsieh, MS, and Ching-yi Wu, ScD, OTR
 Background
.
 
Selection of patients who are most and least likely to benefit from constraint-induced therapy (CIT) for the upper extremity is uncertain.
Objective
. This study investigated demographic and clinical characteristics that may predict outcomes for a distributed form of CIT.
 Methods
. A group of 57 patients were treated with distributed CIT, and 7 potential predictors were identified, including age, sex, side of stroke, time since stroke, spasticity, neurologic status, and movement performance of the distal part of the upper extremity. Treatment outcome was assessed in terms of motor performance, perceived functional ability of the affected hand, and functional performance of daily activities, mea-sured by Fugl-Meyer Assessment (FMA), Motor Activity Log (MAL), and Functional Independence Measure (FIM), respectively.
 Results
. Motor ability of the distal part of the upper extremity and time since stroke were significantly predictive of outcomes on the FMA (adjusted
 R
2
 = 0.18,
P
 = .002) and the MAL subtest quality of movement (adjusted
 R
2
 = 0.43,
P
 < .0001). Motor ability and age were significant predictors of amount of use measured by the MAL (adjusted
 R
2
 = 0.20,
P
 = .001). None of the variables exhibited a predictive relationship with the FIM.
Conclusions
. The best predictor for motor outcomes after distributed CIT was greater motor ability of the distal part of the upper extremity, which is consistent with the presence of residual motor pathways that may respond to training. The FMA may be of value in stratifying patients for their likelihood to benefit from distributed CIT protocols.

Non-prescription portable oxygen concentrators may not be ‘clinically useful

So for your your oxygen needs immediately post stroke make sure your doctor goes the prescription route! Assuming of course that your doctor has an oxygen delivery protocol immediately post stroke to save as many neurons as possible. 

If your doctor is doing nothing about oxygen delivery to the brain s/he is letting more neurons die than should. ARE YOU OK WITH THAT? Mine let 5.4 billion neurons die that first week.

No protocol, you need to fire the complete stroke department, starting with the board of directors.  I would suggest one of these:

Possible solutions: Obviously not vetted coming from me. Don't do them.  I'm not medically trained.

You can look at the years these were reported on and tell how long your hospital has been incompetent.

• Normobaric oxygen (10 posts to January 2020)

• oxygen delivery (4 posts to January 2020)

• brain blood flow (3 posts to April 2019) 

The latest here:

Non-prescription portable oxygen concentrators may not be ‘clinically useful

Key takeaways:

• One out of three non-prescription portable oxygen concentrators was deemed “clinically useful.”
• An FDA-cleared portable oxygen concentrator showed the best performance.

For patients who need ambulatory oxygen, over-the-counter portable oxygen concentrators sold online that do not require a prescription may not be helpful, according to study results published in Respiratory Care.

“My colleagues at the COPD Foundation and I were concerned that patients with COPD who require ambulatory oxygen might purchase OTC (not requiring a prescription) oxygen concentrators, believing that these devices would be appropriate for their use,” Richard Casaburi, PhD, MD, associate chief for research in the division of respiratory and critical care physiology and medicine at Harbor-UCLA Medical Center and professor of medicine at David Geffen School of Medicine at UCLA, told Healio. “However, only one of three of the OTC portable concentrators we tested was potentially of use by patients requiring ambulatory oxygen.”

In this study, Casaburi and colleagues evaluated three OTC portable oxygen concentrators not cleared by the FDA to see if they might be appropriate for patients with hypoxemia.

By using a metabolic simulator that mimics metabolic rates and minute ventilations that might be seen in patients with COPD, researchers assessed oxygen supplementation on alveolar oxygen partial pressure from these devices compared with one FDA-cleared portable oxygen concentrator and a compressed oxygen tank.

Each of the three devices had varying oxygen flow settings. For example, OTC1 had continuous flow from 1 L to 7 L per minute in 1 L per minute increments, whereas OTC2 had single flow of3 L per minute and OTC3 had pulse-dose flow settings that ranged from 1 to 5.

In comparison, the FDA-cleared device had continuous flow at 1 L or 2 L per minute and pulse-dose flow settings that ranged from 1 to 6. Meanwhile the compressed oxygen tank had continuous flow at 1 L to 5 L per minute.

Researchers simulated three different metabolic rates to stimulate progressively higher exertion levels for each device with their specific settings. To mimic minimal exertion, the rate was 350 mL per minute; for moderate exercise, the rate was 850 mL per minute; and for heavy exercise, the rate was 1,200 mL per minute.

During these simulations, researchers evaluated end-tidal partial pressure of oxygen (P_ETO2) for each device to assess them against one another and clarify usefulness.

Through observation of each device, raising the metabolic rate generally meant decreasing P_ETO2, according to researchers.

Results from the simulation showed that when flow from the compressed oxygen gas tank went up, so did P_ETO2. Researchers found comparable increases in P_ETO2 to those observed in the compressed oxygen tank with the FDA cleared device using continuous flow at device settings of 1 L and 2 L per minute, but they noted “somewhat smaller elevations” when using the pulsatile-flow settings.

In terms of the OTC devices, researchers observed that only one (OTC3) may be suitable for patients since it demonstrated meaningful and steady rises in P_ETO2 as flow setting increased. Importantly, these elevations did not reach the same level as the FDA-cleared device at a given flow setting.

There was a modest increase in P_ETO2 with the OTC1 device, but this did not increase further when researchers raised the flow setting. Additionally, researchers found only very small rises in P_ETO2 with the OTC2 device.

“Physicians and respiratory care professionals should inform patients requiring portable oxygen that OTC devices may not meet their oxygenation requirements,” Casaburi told Healio.

This study by Casaburi and colleagues speaks to the growing issue of non-prescribed portable oxygen concentrators being sold online and encourages patients to be cautious when making a purchase, according to an accompanying editorial by Richard D. Branson, MSc, RRT, FAARC, professor in the department of surgery at the University of Cincinnati College of Medicine.

“How common are OTC portable oxygen concentrators? A quick search on Amazon.com yielded 823 results for the search term oxygen concentrator,” Branson wrote. “Many of the results included accessories including cannulas, backpacks, humidifiers, etc, but dozens of portable oxygen concentrators. The price of devices ranged from $200 [to] $700. Of note, a number of devices used model numbers identical to model numbers used by manufacturers of FDA-cleared devices. These are clearly deceptive advertising practices.

“For patients with lung disease requiring long-term oxygen therapy, caveat emptor — let the buyer beware,” he added. “Warning patients, however, is insufficient. We should attempt to prevent the sale of these devices to vulnerable patients.”

For more information:

Richard Casaburi, PhD, MD, can be reached at casaburi@ucla.edu.

Reference:

• Branson RD. Respir Care. 2023;doi:10.4187/respcare.11012.

Comparison of wrist actimetry variables of paretic upper limb use in post stroke patients for ecological monitoring

FYI. What is wrist actimetry?

An actigraph is worn like a watch on the wrist of your non-dominant hand and measures activity through light and movement. Actigraphy data can be very helpful for assessing circadian rhythm disorders such as advanced or delayed sleep phase disorder and insomnia.

i can see almost no use for this, measuring lack of use does nothing to get survivors recovered. Deliver stroke protocols for recovery, that would help a hell of a lot more than useless measurements like this.

 

 

Comparison of wrist actimetry variables of paretic upper limb use in post stroke patients for ecological monitoring

• Gilles Dusfour,
• Denis Mottet,
• Makii Muthalib,
• Isabelle Laffont &
• Karima Bakhti 

Journal of NeuroEngineering and Rehabilitation volume 20, Article number: 52 (2023) Cite this article

• Metrics details

Abstract

Background

To date, many wrist actimetric variables dedicated to measuring the upper limbs (UL) in post-stroke patients have been developed but very few comparisons have been made between them. The objective of this study was to compare different actimetric variables of the ULs between a stroke and healthy population.

Methods

Accelerometers were worn continuously for a period of 7 days on both wrists of 19 post-stroke hemiparetic patients as well as 11 healthy subjects. Various wrist actimetry variables were calculated, including the Jerk ratio 50 (JR50, cumulative probability that the Jerk Ratio is between 1 and 2), absolute (FuncUse30) and relative (FuncUseRatio30) amounts of functional use of movements of the ULs with angular amplitude greater than 30°, and absolute (UH) and relative (UseHoursRatio) use hours.

Results

FuncUse30, FuncUseRatio30, UH, UseHoursRatio and JR50 of the paretic UL of stroke patients were significantly lower than in the non-dominant UL of healthy subjects. Comparing the ratio variables in stroke patients, FuncUseRatio30 was significantly lower than UseHoursRatio and JR50, suggesting a more clinically sensitive variable to monitor. In an exploratory analysis, FuncUseRatio tends to decrease with angular range of motion for stroke patients while it remains stable and close to 1 for healthy subjects. UseHoursRatio, FuncUseRatio30 and JR50 show linear correlation with Fugl-Meyer score (FM), with r² equal to 0.53, 0.35 and 0.21, respectively.

Conclusion

This study determined that the FuncUseRatio30 variable provides the most sensitive clinical biomarker of paretic UL use in post-stroke patients, and that FuncUseHours—angular range of motion relationship allows the identification of the UL behaviour of each patient. This ecological information on the level of functional use of the paretic UL can be used to improve follow-up and develop patient-specific therapy.

Background

Stroke is one of the leading causes of disability worldwide, with a global prevalence rate that has been increasing over the past 30 years [1]. Despite the accumulated research on rehabilitation of the paretic upper limb (UL) following a stroke, a large majority of patients continue to present non-use of paretic UL at the chronic stage which impacts their quality of daily life [2]. Only 5 to 20% of stroke survivors regain sufficient paretic UL function after 6 months [3], which leaves the majority of chronic post stroke patients unable to use their paretic UL in their daily life.

Current methods of quantifying movement of the UL rely primarily on clinical deficit scores such as the Fugl-Meyer (FM) test [4], or on more functional tests like the Wolf Motor Function Test (WMFT), Action Research Arm Test (ARAT) or questionnaires (Motor Activity Log—MAL). More recent work focused on the direct visual observation of stroke patients ULs by hospital practitioners in a clinical environment during 7 days [5]. This work found that the ratio of use activity between the paretic limb and the non-paretic limb is around 0.69 for stroke patients [5] whereas it is 0.95 for healthy subjects (non-dominant/dominant) [Bailey et al., 2014]. The human assessor method used by McLaren [5] has the advantage of identifying with certainty the periods of functional use of the UL as assessed directly by the clinician. However, the time and human resource costs of performing these measurements reduce its applicability to monitor multiple patients, and moreover, limiting observations in a clinical setting might not reflect real life of patients in a home environment.

Alternatively, a commonly used quantitative and objective technique to quantify functional UL movements relies on methods based on actimeters or gyroscopes [Bailey et al., 2014] positioned on the two wrists over a period of time ranging from 2 to 7 days. The functional UL movement results of Bailey's work [6, 7] are based on the calculation of activity counts directly from the acceleration signals originally developed by Uswatte [8]. Bailey derived other variables from the accelerometric measurements, such as use hours based on acceleration thresholds and median bilateral magnitude based on the magnitude of the accelerations measured at each wrist. The correlations of UL activity count with clinical scores such as the FM or the WMFT showed high variability between studies [6, 7]. Although Lang et al. [9] showed a strong correlation (r² = 0.62) between the use hours and the WMFT, a more recent study shows a weaker correlation between the median bilateral magnitude and the FM Score (r² = 0.32) or the WMFT score (r² = 0.34) [10]. Recently, Pan et al. [11] developed new accelerometric variables based on the Jerk, which is the derivative of acceleration. Pan et al. [11] showed that the Jerk ratio (JR) has a very high sensitivity to the amount of UL motion as well as a very high correlation with the median bilateral magnitude. Leuenberger et al. [12] extended the method by using inertial sensors (i.e., accelerometer and gyroscope) to separate functional vs. non-functional UL movements. A functional UL movement occurs when the forearm is oriented horizontally (± 30°), which is usually the case in UL manipulation activities. Leuenberger et al. [12] found excellent correlation of the functional use ratio (FuncUseRatio30) with the box and block (BB) test (r² = 0.9). Lum et al. [13] chose to synchronise accelerometers with video recordings of healthy and hemiparetic subjects performing activities of daily life. The video recordings were used both to accurately measure the amount of functional UL movement in the laboratory over a given period of time and to serve as a basis for labelling actimetric data as functional, non-functional and unknown movement. This labelling was then used to develop several machine learning algorithms to separate functional from non-functional UL movements. Although the activity counts showed low correlation with the video results (r² = 0.57), the machine learning algorithms showed excellent results (r² = 0.81).

The majority of studies on wrist actimetric monitoring of post-stroke patients monitor the quantity of UL movement and its bilateral ratio. While these indicators seem relevant for measuring imbalances between the UL motion, it remains difficult to draw conclusions about the functional imbalance and the physical capacities and limitations of the patients' UL in their ecological environments. Leuenberger's work provides a significant advance by identifying the amount of movement around the horizontal plane with an amplitude of ± 30°. For the first time, it is possible to easily discriminate a "functional" amount of movement in an ecological environment. However, Leuemberger's work required inertial sensors that are relatively expensive and have little energy autonomy. Finally, more recent studies based on artificial intelligence algorithms show promising results in identifying functional motion but require a significant amount of time for manual classification of motion. Moreover, these algorithms do not yet distinguish between movements of different amplitudes. This makes it difficult to identify the physical capabilities and limitations of post-stroke subjects in their ecological environments while it is necessary to turn accelerometer data into clinical meaningful data [14].

In this study we recorded 3D acceleration at each wrist, over a period of 7 days, in the volunteers’ home (ecological) environment. We then adapted and compared different accelerometric variables (UseHours, UseHoursRatio, FuncUse30, FuncUseRatio30 and JR50) between a population of 19 stroke patients and 11 healthy subjects to determine the actimetric variable that has the greatest sensitivity to stroke hemiparesis-related upper limb deficits in order to guide clinical decision making.

More at link.

The Connection Between Depression and Stroke, Experts Weigh In On Why Senator John Fetterman’s Story Is More Common Than You Think

 The stroke hospital treating him completely failed at their job of getting him 100% recovered. 100% recovery and depression won't exist. Solve the correct problem, it's NOT depression post stroke, that is a secondary problem.

The Connection Between Depression and Stroke, Experts Weigh In On Why Senator John Fetterman’s Story Is More Common Than You Think

Hackensack Meridian Neuropsychologists available to speak about the connection between depression and stroke, as the nation marks both Mental Health & Stroke Awareness months in May

27-Apr-2023 1:45 PM EDT, by Hackensack Meridian Health contact patient services

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Pennsylvania Senator John Fetterman made headlines earlier this year when he checked himself into the hospital for the treatment of clinical depression. The mental health struggles happened months after the then Senate candidate suffered a stroke. He recently returned to his job in the Senate, and told Americans 

“I want everyone to know that depression is treatable, and treatment works,” Fetterman said in a statement after his release.

Senator Fetterman isn’t alone. The American Stroke Association says depression is a common side effect of a stroke, sometimes caused by biological changes in the brain. The American Stroke Association (ASA) says more than one-third of post-stroke patients deal with depression. 

Yet, post-stroke depression is widely underdiagnosed and untreated. “It is important for patients and their loved ones to know of the risk of post-stroke depression and recognize its symptoms,” said Elizabeth Kera, Ph.D, Director of Psychology and Neuropsychology at the Neuroscience Institute at Hackensack University Medical Center and Assistant Professor of Neurology at the Hackensack Meridian School of Medicine. “Symptoms to look out for include persistent sad or empty feelings, significant fatigue, lack of motivation, social withdrawal, problems concentrating and sleep disturbances.”

Certain risk factors put stroke patients at a greater risk for post-stroke depression including a previous history of depression, the stroke’s severity, whether it left physical disabilities or cognitive impairments and a lack of family support.  

“In addition to organic causes of post stroke depression, there is certainly the potential for depression with the changes in life circumstances that often come with suffering a stroke including mobility issues, inability to work and the financial strain associated with it,” said Monique Tremaine, Ph.D, director of Neuropsychology at JFK Rehabilitation Institute. “Depression can also come with the different ways a post-stroke patient processes memories, speech and their ability to pay attention.”   

Patients who suffer a stroke on the left side of their brain often have their language processing, like Senator Fetterman, and speech impacted. This inhibits their ability to express their emotions, potentially leading to depression.  A patient who suffers a stroke on the right hemisphere of their brain often becomes isolated because they have a difficult time interpreting their own emotions and the emotions of others. Patients who suffered a right side stroke have difficulty understanding non-verbal communication and understanding nuances like sarcasm.  “With so many factors at play, individuals who experience cognitive changes as well as depression often have to adjust to a new sense of self, which can be quite difficult,” says Dr. Kera.

Depression can make stroke recovery harder as the patients may not feel motivated to work on their recovery.   “It is very important to know the signs of depression and to monitor for them post-stroke so that treatment can begin,” said Yolonda Pickett, M. D., Director of behavioral health for Hackensack University Medical Center.  “Depression can worsen a patient's prognosis and their ability to recover after a stroke, so it is very important to begin treatment for depression as soon as it is recognized."

Treatment for post-stroke depression can include but is not limited to the use of antidepressants, psychotherapy sessions or group stroke support group sessions.

Additionally, a recent study found the relationship works in reverse as well, people with depression are more at risk of having a stroke. People who had symptoms of depression had a 46% greater chance of suffering a stroke than those who had no such symptoms, according to a study led by a Ph.D student at the University of Galway in Ireland, published recently in the journal Neurology. The more symptoms of depression participants reported, the higher their risk of stroke, the researchers reported. For example, those who reported five or more symptoms of depression had a 54% higher risk of stroke than those with no symptoms, researchers said. This can also be tied to Sen. Fetterman’s story as he had previously suffered from depression, before having a stroke, but his Senate office said it became severe in February 2023, months after suffering a stroke.

“The reasons behind this associations is likely multifaceted and complicated, but contributing factors may include certain medications for depression can alter a patient’s blood pressure, and in some cases an association between depression and risk factors such as poor diet, lack of exercise, and alcohol use all of which can increase a person’s stroke risk,” Dr. Tremaine said.

As the nation marks both mental health awareness month and stroke awareness month this May, Hackensack Meridian neurologists and neuropsychologists can address the trending topic of the connection between stroke and depression, and what patients and their families can do to mitigate their risks for both stroke and depression.

Can Working Long Hours Increase Your Risk of a Stroke?

FYI.

 

Can Working Long Hours Increase Your Risk of a Stroke?

27-Apr-2023 4:20 PM EDT, by Hackensack Meridian Health contact patient services

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Every 40 seconds, someone in the United States has a stroke. Every 3.5 minutes, someone dies of stroke. 

Experts agree, anyone can have a stroke at any age. But certain risk factors, like high cholesterol, high blood pressure, diabetes, and obesity, can increase your chances of having a stroke. Now add to this list the possibility of working long hours! That’s according to a new study that found people, particularly those under age 50, have a higher risk of stroke when working long hours for a decade or more. 

The research, published in the American Heart Association's journal Stroke, found that participants working long hours had a 29% greater risk of stroke, and those working long hours for 10 years or more had a 45% greater risk of stroke.

“Stress can cause the heart to work harder and increase blood pressure,” says Martin Gizzi, MD, PhD, Vice Chair of Neurology and Director, Cerebrovascular Diseases Program at Hackensack University Medical Center, who explains that this can increase the risk of a blood clot forming, traveling to the brain and causing a stroke. “If this happens, it is important for people to recognize the signs of a stroke because time is of the essence.”

Dr. Gizzi says while signs of a stroke can vary - and include sudden numbness or weakness in the face, arm or leg; sudden confusion or trouble speaking; trouble seeing; and a sudden loss of coordination, one thing is for sure - seek medical attention quickly in the event of any of them.

“With each passing minute, more brain cells are damaged but luckily, we have effective treatments that can make a big difference and in some cases, even reverse the stroke symptoms,” says Dr. Gizzi. The time to initiate these treatments for an acute ischemic stroke, the most common type of stroke, has generally been limited to within 4.5 hours after the onset of symptoms. But recently, this window was expanded at a small number of hospitals. 

“The benefits of tPA, the drug used to break up a blood clot and restore blood flow to the brain, can now be extended to 9 hours past the onset of stroke symptoms,” says Dr. Gizzi. “Advanced imaging technology is required, but when results are optimal, this is twice the time window!”

Dr. Gizzi says while it’s still crucial to treat a stroke as soon as possible, this expanded window for treatment could be a life-saving change for some people who suffer strokes.

This May, National Stroke Awareness Month, please consider exploring a story on these  developments that can have an impact on so many lives. 

Music to Your Ears and Brain: Long-Term Musical Training Can Keep Your Brain Young

Well, your stroke doctor will do nothing with this. They have done nothing with all this earlier research on music helping stroke recovery so why do anything with this. 

Does your hospital or doctor have ANY PROTOCOL  on music for your rehab?

• music (94 posts back to March 2011)

• music therapy (53 posts back to October 2014)

• musical training (13 posts back to June 2014)

 

Why not?

Your doctors' and hospitals' reasons for doing nothing? There is absolutely no excuse for doing nothing.

Laziness? Incompetence? Or just don't care? No leadership? No strategy? Not my job? Not my Problem?

Music to Your Ears and Brain: Long-Term Musical Training Can Keep Your Brain Young

Summary: A new study shows that musical training can improve audiovisual speech perception in aging adults by preserving and compensating for youthful neural patterns.

The research reveals two mechanisms that older musicians use to counteract age-related decline: functional preservation and functional compensation, providing hope for targeted interventions to promote healthy aging.

Source: Chinese Academy of Science

The world’s population is aging at an unprecedented rate. Aging can lead to various types of cognitive decline, posing a serious burden to families and society. Therefore, it is crucial to develop effective interventions to promote healthy aging.

One promising approach is musical training, which is accessible to the majority of the population. Besides the musically rewarding and aesthetic experience of musical training, it also provides potential benefits to the brain, especially for the elderly.

In a study published as a cover story in Science Advances, a research team led by Dr. DU Yi from the Institute of Psychology of the Chinese Academy of Sciences found that long-term musical training could mitigate and even counteract age-related decline of audiovisual speech-in-noise perception in older listeners, through functional preservation of youth-like activity patterns in sensorimotor areas, supplemented by functional compensation in frontoparietal and default mode network (DMN) regions.

Older musicians, older non-musicians, and young non-musicians participated in this neuroimaging study.

The researchers found that older musicians outperformed older non-musicians and even equaled young non-musicians in identifying audiovisual syllables under noisy conditions. By analyzing their brain activity, the researchers revealed two mechanisms that old musicians adopt to counteract aging: functional preservation and functional compensation.

Specifically, older musicians retained neural specificity of speech representations in sensorimotor areas at a level similar to young non-musicians, while older non-musicians showed degraded neural representations.

In the same region, older musicians showed higher neural alignment (i.e., higher pattern similarity) in comparison to young non-musicians than older non-musicians did, and this capacity was associated with the older musicians’ training intensity. Importantly, youth-like brain function predicted better audiovisual speech-in-noise perception performance in older adults.

In addition, the researchers found that older musicians, in comparison with older non-musicians, also showed greater activation in frontoparietal regions that support multiple tasks across domains and greater inhibition in task-irrelevant DMN regions that help avoid interference.

The greater DMN deactivation predicted better audiovisual speech-in-noise performance. Furthermore, these two mechanisms are interdependent, as greater frontoparietal activation and greater DMN inhibition contributed to more similar neural patterns in sensorimotor regions in older adults. In other words, functional compensation further supported functional preservation.

The researchers found that older musicians outperformed older non-musicians and even equaled young non-musicians in identifying audiovisual syllables under noisy conditions. Credit: Neuroscience News via DALL-E 2

“Playing music makes older adults better listeners by preserving youthful neural patterns as well as recruiting additional compensatory brain regions. Our study provides empirical evidence to support that playing music keeps your brain sharp, young, and focused,” said Dr. DU, corresponding author of this study.

This study provides insights into adaptive brain reorganization in aging populations and how lifelong musical training leads to “successful aging” in speech processing by preserving youthful brain characteristics and enhancing compensatory brain scaffolding.

The functional preservation of sensorimotor regions along with compensatory DMN deactivation also suggest avenues for more targeted training regimens to protect speech functions in the elderly.

About this music and brain aging research news

Author: LIU Chen
Source: Chinese Academy of Science
Contact: LIU Chen – Chinese Academy of Science
Image: The image is credited to Neuroscience News

Original Research: Open access.
“Successful Aging of Musicians: Preservation of Sensorimotor Regions Aids Speech-in-noise Perception” by DU Yi et al. Science Advances

Glaucoma Drugs Prevent Cognitive Impairment Associated With Alzheimer’s Disease in Mice

 FYI. Will your doctors and stroke hospital ensure human testing gets done? NO? Then you don't have a functioning stroke doctor or hospital. With your risk of dementia you need prevention solutions from your doctor.

Your risk of dementia, has your doctor told you of this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018

The latest here:

Glaucoma Drugs Prevent Cognitive Impairment Associated With Alzheimer’s Disease in Mice

Summary: Drugs used to treat glaucoma and high-altitude sickness may prevent cognitive impairment caused by Alzheimer’s disease in mice. The research indicates that carbonic anhydrase inhibitors, already approved by the US Food and Drug Administration (FDA), promote the clearance of amyloid beta from blood vessels and glial cells, which control brain inflammatory processes, as well as reducing inflammation, restoring cell function and preventing cognitive impairment.

Key Points:

1. A new study shows that glaucoma drugs prevent cognitive impairment associated with Alzheimer’s disease in mice.
2. The drugs promote the clearance of amyloid beta from blood vessels and glial cells, reducing inflammation, restoring cell function, and preventing cognitive impairment.
3. Clinical trials to test the effectiveness of these drugs against Alzheimer’s disease in humans could be underway soon as they are already approved by the FDA.

Source: Temple University Health System

Changes in blood vessels in the brain linked to the build-up of a sticky protein known as amyloid beta are a hallmark of early-stage Alzheimer’s disease.

As amyloid accumulates on the walls of vessels, brain cells lose nutrients and oxygen, becoming inflamed and dysfunctional. Over time, this gives rise to cerebral amyloid angiopathy (CAA), a major cause of aging-related cognitive decline.

Reversing the effects of CAA and neuroinflammation could bring significant benefits for individuals at risk of Alzheimer’s disease – and now, new research at the Lewis Katz School of Medicine at Temple University brings that hope within reach.

In experiments carried out in mice, the Temple scientists show that drugs known as carbonic anhydrase inhibitors (CAIs), already FDA-approved for other conditions, such as glaucoma and high-altitude sickness, promote the clearance of amyloid beta from blood vessels and glial cells, which control brain inflammatory processes.

In doing so, CAIs not only reduce inflammation and restore cell function but also prevent cognitive impairment.

The study took place in the lab of Silvia Fossati, PhD, Associate Professor of Neural Sciences and Cardiovascular Sciences at the Lewis Katz School of Medicine at Temple University, and is the first to test the FDA-approved CAIs acetazolamide and methazolamide in animals with cerebrovascular alterations mimicking those of CAA and Alzheimer’s disease in humans.

The results appeared online in the journal Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

“Cognitive impairment is closely associated with damage to blood vessels and inflammation in the brain, which are among the main causes, but also consequences, of amyloid accumulation,” explained Dr. Fossati, who is also Associate Director of the Alzheimer’s Center at Temple’s Katz School of Medicine.

“We wanted to see if we could prevent cerebrovascular dysfunction, inflammation and improve cognitive function by therapeutically improving the health of vascular and glial cells, thereby facilitating the removal of amyloid from blood vessels and the brain tissue.”

In previous work, Dr. Fossati and colleagues found that amyloid accumulation causes mitochondria – the energy-generating powerhouses of cells – to function abnormally and that this process is linked to activity of the enzyme carbonic anhydrase.

“We also know from experiments in cells that CAIs suppress mitochondrial dysfunction and cell death induced by amyloid,” Dr. Fossati said. “But whether these same effects occur in vivo has been unknown.”

To test CAIs in vivo, Dr. Fossati and colleagues used a mouse model in which animals, as they age, exhibit increasing levels of human amyloid protein in the brain. As amyloid deposits accumulate in the brain vasculature, the animals begin to show signs of cerebrovascular dysfunction, similar to the way in which humans develop signs of CAA.

The animals were treated with either acetazolamide or methazolamide from about 8 months of age, when signs of amyloid pathology first emerge in these animals, until about 15 or 16 months, when advanced cognitive impairment is present.

When the researchers examined brain tissue from CAI-treated mice, they found significant reductions in amyloid in the cerebral vasculature and in glial cells. They also found that glial cells and blood vessels were overall healthier and had better amyloid-clearing capacity compared to untreated animals.

“Both acetazolamide and methazolamide were highly effective in reducing amyloid deposition and in improving cerebrovascular function,” Dr. Fossati said.

Reversing the effects of CAA and neuroinflammation could bring significant benefits for individuals at risk of Alzheimer’s disease. Credit: Neuroscience News

“Our behavioral studies showed that, as Alzheimer’s pathology decreased, CAI-treated mice experienced noticeable gains in cognitive function.”

Additional analyses focused on post-mortem human brain tissue from Alzheimer’s patients. These analyses showed that, similar to animals, levels of a specific carbonic anhydrase enzyme found in mitochondria are abnormally elevated in the brains of Alzheimer’s disease and CAA patients. The evidence is the first to identify carbonic anhydrase as a key factor in humans affected by these conditions.

The group plans next to design and investigate CAIs that are more specific to mitochondria, with the help of Marc Ilies, PhD, Professor in the Department of Pharmaceutical Sciences at the Temple School of Pharmacy.

“The therapies we used for the current study target carbonic anhydrases in the whole cell,” Dr. Fossati explained. “If we can target the enzyme specifically within mitochondria, the efficacy of therapy could improve greatly, and side effects could be reduced.”

Nonetheless, clinical trials to test the effectiveness of acetazolamide and methazolamide against CAA in humans could be underway soon, as both agents are already approved by the FDA.

Other researchers who contributed to the new study include Elisa Canepa, Rebecca Parodi-Rullan, Rafael Vazquez-Torres, Roberto Guzman-Hernandez, Nicole L. Lemon, and Federica Angiulli, Alzheimer’s Center at Temple, Department of Neural Sciences, Lewis Katz School of Medicine; Begona Gamallo-Lana and Adam C. Mar, Department of Neuroscience and Physiology, Neuroscience Institute, NYU Grossman School of Medicine; Ludovic Debure and Thomas Wisniewski, Department of Neurology, Center for Cognitive Neurology, NYU Grossman School of Medicine; Marc A. Ilies, Department of Pharmaceutical Sciences and Moulder Center for Drug Discovery Research, Temple University School of Pharmacy; and Leif Østergaard and Eugenio Gutiérrez-Jiménez, Center of Functionally Integrative Neuroscience (CFIN), Department of Clinical Medicine, Aarhus University, Denmark.

Funding: Funding was provided in part by grants from the National Institutes of Health, the Edward N. and Della L. Thome Memorial Foundation Awards Program in Alzheimer’s Disease Drug Discovery Research, the Alzheimer’s Association, the Pennsylvania Department of Health Collaborative Research on Alzheimer’s Disease (PA Cure), the Karen Toffler Charitable Trust, and the Lemole Center at Temple.

About this neuropharmacology research news

Author: Jeremy Walter
Source: Temple University Health System
Contact: Jeremy Walter – Temple University Health System
Image: The image is credited to Neuroscience News

Original Research: Open access.
“FDA-approved carbonic anhydrase inhibitors reduce amyloid β pathology and improve cognition, by ameliorating cerebrovascular health and glial fitness” by Silvia Fossati et al. Alzheimer’s & Dementia

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Abstract

FDA-approved carbonic anhydrase inhibitors reduce amyloid β pathology and improve cognition, by ameliorating cerebrovascular health and glial fitness

Introduction

Cerebrovascular pathology is an early and causal hallmark of Alzheimer’s disease (AD), in need of effective therapies.

Methods

Based on the success of our previous in vitro studies, we tested for the first time in a model of AD and cerebral amyloid angiopathy (CAA), the carbonic anhydrase inhibitors (CAIs) methazolamide and acetazolamide, Food and Drug Administration–approved against glaucoma and high-altitude sickness.

Results

Both CAIs reduced cerebral, vascular, and glial amyloid beta (Aβ) accumulation and caspase activation, diminished gliosis, and ameliorated cognition in TgSwDI mice. The CAIs also improved microvascular fitness and induced protective glial pro-clearance pathways, resulting in the reduction of Aβ deposition. Notably, we unveiled that the mitochondrial carbonic anhydrase-VB (CA-VB) is upregulated in TgSwDI brains, CAA and AD+CAA human subjects, and in endothelial cells upon Aβ treatment. Strikingly, CA-VB silencing specifically reduces Aβ-mediated endothelial apoptosis.

Discussion

This work substantiates the potential application of CAIs in clinical trials for AD and CAA.

Quantifying Nonuse in Chronic Stroke Patients: A Study Into Paretic, Nonparetic, and Bimanual Upper-Limb Use in Daily Life

Damn it all, it is NOT learned nonuse. It is the actual inability to use it because of dead neurons. Quit blaming the patient for not recovering and blame the doctor and therapists for knowing nothing on how to get survivors recovered! 

Do you blithering idiots ever actually think about why stroke patients don't recover?

Quantifying Nonuse in Chronic Stroke Patients: A Study Into Paretic, Nonparetic, and Bimanual Upper-Limb Use in Daily Life

Marian E. Michielsen, MSc
†
 , Ruud W. Selles, PhD, Henk J. Stam, MD, PhD Gerard M. Ribbers, MD, PhD, Johannes B. Bussmann, PhD
ABSTRACT. Michielsen ME, Selles RW, Stam HJ, RibbersGM, Bussmann JB.  Arch Phys Med Rehabil 2012;xx:xxx.
Objective:
 To quantify uni- and bimanual upper-limb use inpatients with chronic stroke in daily life compared with healthy controls.
Design:
 Cross-sectional observational study.
Setting:
 Outpatient rehabilitation center.
Participants:
 Patients with chronic stroke (n

38) and healthycontrols (n

18).
Intervention:
 Not applicable.
Main Outcome Measures:
 Upper-limb use in daily life was measured with an accelerometry-based upper-limb activity monitor, an accelerometer based measurement device. Uni-manual use of the paretic and the nonparetic side and bimanual upper-limb use were measured for a period of 24 hours. Outcomes were expressed in terms of both duration and intensity.
Results:
 Patients used their unaffected limb much more than their affected limb (5.3h vs 2.4h), while controls used both limbs a more equal amount of time (5.4h vs 5.1h). Patients used their paretic side less than controls used their nondominant side and their nonparetic side more than controls their dominant side. The intensity with which patients used their paretic side was lower than that with which controls used their nondominant side, while that of the nonparetic side was higher than that of the dominant side of controls. Finally, patients used their paretic side almost exclusively in bimanual activities. During bimanual activities, the intensity with which they used their affected side was much lower than that of the nonaffected side.
Conclusion:
 Our data show considerable nonuse of the paretic side, both in duration and in intensity, and both during unimanual and bimanual activities in patients with chronicstroke. Patients do compensate for this with increased use of the nonparetic side.
Key Words:
 Ambulatory monitoring; Motor activity; Reha-bilitation; Stroke; Upper extremity.©
 2012 by the American Congress of Rehabilitation Medicine
F
IFTY TO 70% OF PATIENTS with stroke suffer fromlong-term motor deficits of the upper limb,
1
with a de-creased use of the paretic upper extremity in daily life.
2
Be-cause this latter may have a great impact on the manner inwhich a patient is able to participate in daily life activities,maximizing purposeful use of the upper extremity in daily lifeis a key factor in motor rehabilitation following stroke.While it is clear that a decreased motor capacity of theparetic arm influences the use of both extremities, the exactchanges in upper-limb use following stroke are not yet fullyunderstood. Regarding the paretic upper extremity, many studies have shown that there is no 1-on-1 relation between motor impairment and functional use.
3,4
This may be related to the phenomenon of learned nonuse,
5
which describes how patients will have “learned” not to use the paretic side to its fullcapacity.
6
Brain injury causes structural damage to motor path-ways as well as depression of neural excitability near thelesion. Decreasing activity of the upper extremity leads to afurther reduction in excitability and as such starts a viciouscircle of decreasing excitability and decreasing activity.
7
Even less is known about the consequences of stroke on thenonparetic side. Motor performance of the nonparetic side maybe impaired compared with that in healthy subjects, showing,for instance, decreased speed and consistency of performance.
8
In addition, it has been shown that patients with acute strokehave a more reduced use of the nonparetic side in daily life thando healthy subjects.
9
On the other hand, it is generally assumedthat poststroke the nonparetic side will be used more to com-pensate for the decreased use of the paretic side. However, toour knowledge, this has not been investigated in patients withchronic stroke.Overall many questions on techniques to optimize the func-tion of the paretic extremity after stroke still need to be an-swered. The optimal rehabilitation technique is still not de-fined, and different approaches in reducing upper-extremityparesis are distinguished.
7
Several therapies have been devel-oped to improve the use of the nonparetic arm in daily life. Forexample, constraint-induced movement therapy (CIMT),
10,11
or forced use,
12
reported as a beneficial treatment option formotor recovery of the arm,
13
prevents the use of the nonpareticupper limb and aims to counterbalance the learned nonuse.CIMT is an augmentative technique,
7
a high-intensity, uni-manual training aiming to counterbalance the vicious circle of decreasing excitability and decreasing activity. Furthermore,CIMT has aspects of task-specific exercising. Bilateral trainingprograms have also been developed, for example, with rhythmic
 auditory cueing.
14
To evaluate and understand the effects of upper-extremity training in daily life conditions, detailed insight isneeded in unimanual and bimanual function of the arms in dailylife conditions. This is the topic of the current article.Several studies have included the measurement of upper-limb use in daily life. For example, Taub,
11
Mark,
15
and Wolf
5
and colleagues used the Motor Activity Log (MAL) in their studies. However, although validated against an objective mea-sure,
16
the MAL still is a subjective instrument that focuses on how well and how much patients use their most impaired arm in a defined category of activities, and the MAL does not include data on the amount of use of the non impaired arm and bilateral use. Another method for assessing upper-limb use in a home setting is provided by accelerometers and other portable devices providing the opportunity to assess how much patients with stroke use their upper limbs in daily life for longer periods.
2
However, so far, studies using these devices assessed only the upper-limb use overall and not in detail. For example,many studies express actual upper-limb use only as a ratio between the use of the affected and the use of the unaffected side,
17
thus omitting information about usage times of the paretic side and the nonparetic side separately. Second, currentdevices do not differentiate between arm movements resulting from general body movements such as walking and arm movements during sitting and standing. Third, most measurement devices cannot differentiate between the duration of use and the intensity of use, and finally, most devices cannot or do not differentiate between unilateral and bilateral usage of the arms.The aim of the present study was to quantify uni- and bimanual upper-limb use in patients with chronic stroke in daily life and compare this with healthy controls. By using an accelerometry based upper-limb activity monitor,
18
we were able to give an insight into both duration and intensity of upper-limb use and to discriminate between upper-limb movements caused by whole-body movements and movements independent of whole-body movements, thus providing an insight into the amount of functional and purposeful upper-limb use in daily life conditions.

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Empowering stroke survivors: understanding the role of multidisciplinary rehabilitation Impact of stroke

Multidisciplinary teams  KNOW NOTHING ABOUT 100% RECOVERY!  Ask them! I consider them pretty much useless. 

Oops, I'm not playing by the polite rules of Dale Carnegie;  'How to Win Friends and Influence People'. 

Telling supposedly smart stroke medical persons they know nothing about stroke is a no-no even if it is true. 

Politeness will never solve anything in stroke. Yes, I'm a bomb thrower and proud of it. Someday a stroke 'leader' will try to ream me out for making them look bad by being truthful, I look forward to that day. 

 The latest invalid chest thumping here:

 

Empowering stroke survivors: understanding the role of multidisciplinary rehabilitation Impact of stroke

• Urvashy Gopaul, PhD, MSc
• Demers Marika
• Marina Charalambous
• William R Reed

Published:April 24, 2023DOI:https://doi.org/10.1016/j.apmr.2022.12.199

Stroke is one of the leading causes of disability worldwide, with someone having a stroke every 40 seconds in the United-States[1]. A stroke can occur by clot that interrupts blood flow in the brain. It can also be caused by a burst of a blood vessel that causes bleeding in the brain. There are also other unknown causes of stroke which occur less frequently. A stroke causes brain cells to die as they no longer receive oxygen and nutrients from the blood. Some of the most common risk factors of stroke are high blood pressure, high cholesterol, heart diseases, diabetes, smoking, physical inactivity, and obesity[2]. Unfortunately, one in three adults has at least one of these conditions or habits[1].

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Gait training with a wearable powered robot during stroke rehabilitation: a randomized parallel-group trial

'May' is NOT GOOD ENOUGH! Do the research that delivers results! Survivors want results, not milquetoast options.

Gait training with a wearable powered robot during stroke rehabilitation: a randomized parallel-group trial

• Daichi Miyagawa,
• Akira Matsushima,
• Yoichi Maruyama,
• Noriaki Mizukami,
• Mikio Tetsuya,
• Minoru Hashimoto &
• Kunihiro Yoshida 

Journal of NeuroEngineering and Rehabilitation volume 20, Article number: 54 (2023) Cite this article

• Metrics details

Abstract

Background

We have developed a wearable rehabilitation robot, “curara®,” and examined its immediate effect in patients with spinocerebellar degeneration and stroke, but its rehabilitative effect has not been clarified. The purpose of this study was to examine the effect of this device on gait training in stroke patients.

Methods

Forty stroke patients were enrolled in this study. The participants were divided randomly into two groups (groups A and B). The participants assigned to group A received RAGT with curara® type 4, whereas those in group B received conventional therapist-assisted gait training. The clinical trial period was 15 days. The participants performed 10 sessions of gait training (5 times per week) each lasting 30 ± 5 min per day. The 10-m walking time (10mWT), and 6-minute walking distance (6MWD) were evaluated as the main outcomes. Timed up and go and Berg Balance Scale (BBS) were also examined. Gait parameters (stride duration and length, standard deviation of stride duration and length, cadence, ratio of the stance/swing phases, minimum/maximum knee joint angle, and minimum/maximum hip joint angle) were measured using a RehaGait®. The items other than BBS were measured on days 0, 7, and 14, whereas BBS was measured on days 0 and 14. The improvement rate was calculated as the difference of values between days 14 and 0 divided by the value on day 0. The improvement rates of the 10mWT and 6MWD were set as the main outcomes.

Results

The data of 35 participants were analyzed. There was no significant difference in the main outcomes between both groups at the end of gait training. As for intragroup changes, gait speed, stride length, stride duration, and cadence were improved significantly between days 0 and 14 in each group. When examining the interaction effect between the day of measurement and group, stride duration (p = 0.006) and cadence (p = 0.012) were more significantly improved in group A than in group B.

Conclusions

This novel wearable powered robot may have the potential to improve gait speed of individuals in stroke rehabilitation.

Trial registration

Japan Registry of Clinical Trials (jRCTs032180163). Registered on February 22, 2019; https://jrct.niph.go.jp/en-latest-detail/jRCTs032180163.

UMIN Clinical Trials Registry (UMIN000034237)

Registered on September 22, 2018; https://center6.umin.ac.jp/cgi-open-bin/icdr/ctr_view.cgi?recptno=R000038939.

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