Browsed by
Category: Brain disease

Analyze the links between BMI, obesity & cognitive ability.

Analyze the links between BMI, obesity & cognitive ability.

Comments 0 Comment

According to the World Health Organisation (WHO), there were more than 650 million obese adults in the world as of 2016. Obesity has been linked in the past to an increased risk of cognitive deterioration.

Evidence from University College London researchers challenges the idea that fat and cognitive capacity are causally related.

Around the world, more than 1.9 billion adults were obese in 2016, with more than 650 million of those adults suffering from obesity, a disease in which a person’s weight is over normal ranges and may lead to various health issues.

According to current estimates, 167 million adults and children will be overweight or obese by 2025. A multitude of disorders, including diabetes, cardiovascular disease, hypertension, osteoporosis, rheumatoid arthritis, and cancer, have been linked to obesity in previous studies, including these.

Furthermore, previous research has connected obesity to a higher risk of cognitive deterioration.

The causal relationship between obesity and cognitive performance has now been called into question by University College London academics. They contend that common family variables have tainted the research linking cognitive aptitude and BMI.

Obesity

If a person’s present weight is excessive for their height, they are considered obese. The body mass index (BMI) is the most popular metric for determining a person’s level of obesity.

This tool determines if an adult is obese or not based on their height and current weight:

  • BMI less than 18.5 indicates underweight.
  • Suitable BMI range: 18.5-24.9
  • BMI of 25 to 29.9 indicates obesity
  • obesity: a BMI of 30 or above

Children and teenagers need a different BMI calculator, which considers height, age, and gender to evaluate obesity because they are still developing.

The BMI measurement is not without problems, though. It is unable to distinguish between muscle and fat when weighing someone. Additionally, it disregards a person’s race, overall body composition, or bone density.

Cognitive function and obesity

Lead author of this study and senior research fellow at the Centre for Longitudinal Studies at University College London in the U.K., Dr. Liam Wright, Ph.D., states that there are several reasons why the research team decided to investigate the causal relationship between cognitive capacity and obesity:

“Over the past forty years, there has been a significant rise in the prevalence of obesity, but BMI hasn’t increased uniformly throughout the population. Therefore, it is crucial to understand why some people are more predisposed to obesity than others.

Additionally, there is a substantial body of research in the field of cognitive epidemiology that demonstrates a connection between cognitive function and practically every measure of health and health behaviour, including obesity.

Unfortunately, the majority of the cognitive epidemiology literature employs observational research designs that may be biassed and fail to show causal effects, according to Dr. Wright. “There are some compelling theoretical arguments for why cognitive ability might have a causal effect on health, but regrettably, these arguments are based on observational research designs,” she said. Because a sibling design could take into account some of the variables that can skew relationships found in previous research, we felt it was crucial to investigate for a relationship between cognitive capacity and BMI.

Examining siblings to reduce bias

Dr. Wright and his research group evaluated data from four distinct young population cohort studies carried out in the United States that included 12,250 siblings from 5,602 homes. Each participant’s data were tracked from youth to age 62.

The scientists were able to take into consideration unobserved characteristics associated with family background by analysing the relationship between cognitive capacity and BMI among families.

“Sibling designs account for factors that are shared between siblings by design,” Dr. Wright said. They don’t require the measurement of these factors, which is both a benefit and a drawback because it is difficult to determine which common factors actually contribute.

With this qualification, he continued, “There are four main factors that we thought might be significant: genetics (siblings share 50% of DNA), parental socioeconomic class (wealth, location, etc.), parenting styles (particularly regarding dietary choices), and parental cognitive ability (cognitive ability could operate indirectly!). “Once more, we didn’t directly examine these.”

According to Dr. Wright, they predicted that these variables would make general population studies more biassed and lead to weaker relationships than in earlier studies, which is exactly what they found.

However, he cautioned, “remember that sibling designs have their own flaws, including the ability for siblings to influence one another, for example, by modelling one another’s behaviour. This may imply that our findings are also skewed, albeit downwardly and smaller than the actual causal effect.

Association between BMI and cognitive ability

When the researchers evaluated the data from study participants who were not related, they discovered that, after accounting for family socioeconomic status, the change in teenage cognitive capacity from the 25th to the 75th percentile was associated with an estimated 0.61 kg/m drop in BMI.

And when the researchers analyzed the information from siblings, they discovered that the change in BMI from the 25th to the 75th percentile of teenage cognitive ability was only correlated with a 0.06 kg/m drop in cognitive capacity.

The relationship between cognitive capacity and BMI was less pronounced when siblings were compared than when the entire population was, according to Dr. Wright, but he was not surprised by this given the overall characteristics he mentioned.

However, he noted, “I was shocked at how little of an association there was when comparing siblings. As said, there are strong arguments to support the idea that cognitive ability has an impact on health and health-related decision-making“.

“Two possibilities for this small association are that one, our results were biassed towards finding smaller associations (e.g., by siblings influencing each other), and two, reflective decision-making isn’t as important in determining BMI as other factors like satiety, etc.,” Dr. Wright continued. Both of these are hypothetical.

Unproven causality

As a parent and a neurologist, Dr. Segil claimed that he has never observed a connection between obesity or a healthy weight and cognitive aptitude in people.obese

The purpose of this study, according to Dr. Segil, “is to argue that people with higher cognitive abilities, who have a higher socioeconomic position, have made healthier decisions.” Additionally, it’s possible that people’s cognitive function increases as their BMI decreases when they make healthier decisions.

He continued, “I do not believe that there is any evidence linking obesity to cognitive function. And I believe that their research’s use of siblings or other family members who are in a similar social economic situation to real-life situations such as brothers or sisters or siblings is realistic.”

After reading this study, Dr. Segil stated that he would be curious to know whether maternal or paternal obesity had a greater impact on adolescent cognitive development.

As a result of reading this, they claimed that adolescent cognition is linked to a lower adult BMI, he continued. So I’m keen to know if stronger adolescent cognitive abilities are related to the maternal and paternal BMI. Does having a thin or fat parent, using the same dataset, alter their children’s cognitive ability?I was shocked, though, by how little of an association there was when comparing siblings. As mentioned, there are strong arguments to support the idea that cognitive ability has an impact on one’s health and decision-making in relation to their health.

RFERENCES:

For Cognitive disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_478

New clues about how ketamine could lead to psychosis.

New clues about how ketamine could lead to psychosis.

Comments 0 Comment

Researchers looked into whether ketamine could cause mental changes like psychosis. They discovered that ketamine increases ambient noise, which may obstruct the brain’s ability to process sensory signals.

As rats were used in the study, more research is required to determine whether the results apply to people. Changes in reality perception, such as persistent delusions, hallucinations, and disorganized thought, are characteristics of schizophrenia. Almost 24 million people around the world are affected by the illness.

There is still no known cause for schizophrenia. Yet, research points to environmental, psychological, and genetic variables as potential causes of the illness.

By blocking NMDA receptors in the brain, the drug ketamine causes a mental state resembling psychosis in healthy humans. As a result, the central nervous system develops an imbalance of excitatory and inhibitory signals, which impacts sensory experience.

According to experts, schizophrenia-related perception abnormalities may be related to similar changes in NMDA receptors. Yet, it hasn’t been made clear how this might be the case.

Ketamine and psychosis

Recently, scientists investigated how ketamine alters sensory perception in rat brains.

They discovered that ketamine increased “background noise” in the brain, which reduced the clarity or intensity of sensory information. They remarked that this might help to explain why persons with schizophrenia or psychosis experience reality differently. The European Journal of Neuroscience published their findings.

These results, according to Dr. Sam Zand, a Las Vegas-based psychiatrist who was not involved in the study, “indicate that malfunction in NMDA receptors may play a role in the development of psychosis.”

“The work offers fresh understandings into the process by which ketamine may cause psychotic symptoms. The results might influence the creation of novel medications for psychosis that target NMDA receptors or brain noise, the researcher continued.

Study design

Seven male lab rats were used in the study to examine how ketamine affected their ability to perceive sensory information. To do this, they first implanted electrodes into rats’ brains to capture electrical activity.

They then recorded the brain’s reactions before and after administering ketamine while simulating their own whiskers. To be more precise, the scientists studied how ketamine affected beta and gamma oscillations in a neuronal network. They carries messages from sensory organs to the brain.

Gamma waves have a frequency range of 30-80 Hz, while beta oscillations have a frequency range of 17-29 Hertz (Hz). Processing sensory data requires the use of frequencies.

In the end, the scientists discovered that even before they stimulated the rats’ whiskers, ketamine enhanced power in both beta and gamma oscillations.

However, they also discovered that the amplitude of the rats’ beta and gamma oscillations dropped post-stimulus and after ketamine administration, which is associated with hampered perception.

They also observed that ketamine enhanced gamma frequency noise, which is related to a reduced capacity for sensory signal processing.

The researchers hypothesised that their findings suggest that increased background noise, which in turn may be brought on by damaged NMDA receptors leading to an imbalance of inhibition and excitation in the brain, may be a trigger for the distorted reality experienced in psychosis and schizophrenia.

According to Dr. Sofya Kulikova, senior research fellow at the HSE University in Perm, Russia, and one of the study’s authors, “The discovered alterations in thalamic and cortical electrical activity associated with ketamine-induced sensory information processing disorders could serve as biomarkers for testing antipsychotic drugs or predicting the course of disease in patients with psychotic spectrum disorders.”

Research limitations

The study was not conducted by Dr. Howard Pratt, a psychiatrist and mental health medical director at Community Health of South Florida. He made it clear that:

The main drawback of these results is that, although a strong association, causation has not yet been shown. There are many potential explanations for conditions like psychosis, including increases in dopamine, which is the focus of treatment for those with a diagnosis of schizophrenia. I’m interested to see what happens as the investigation expands past animal studies.

We also discussed the study’s shortcomings with Dr. James Giordano, the Pellegrino Institute professor of neurology and biochemistry at Georgetown University Medical Center who was not engaged in the study.

The fact that the study solely looked at ketamine-induced effects, he said, “is a key limitation. While valuable and practical for understanding ketamine’s activity in a rat model, it may not provide direct translation to comprehend non-drug-induced dissociative, and psychotic states in humans.”

Dr. Giordano went on to say that it is possible that the effects of ketamine on humans, while undoubtedly dissociative and exhibiting some psychotic traits, are not entirely representative of or identical to the neurological mechanisms underlying other forms of psychosis and schizophreniform disorders.

Possible clinical repercussions

The study’s ramifications, according to Dr. Giordano, are that “[t]hese findings are useful in that evidence of ketamine’s actions at defined brain networks may enable better understanding— and improved clinical applications—of its effects in humans.”

The researcher added, “In addition, by highlighting the functions of these brain nodes and networks involved in mediating dissociative experiences, we may create improved understanding — and possibly treatments for — specific types of drug-induced psychoses, and perhaps other psychotic illnesses, such as forms of schizophrenia, as well.

Larger Trials Needed

Dan Iosifescu, MD, MSc, associate professor of psychiatry at New York University School of Medicine in New York City, commented on the study and said that if the results “were based on a larger study” it would be very important because such patients are currently being denied access to a beneficial treatment due to a theoretical risk of psychosis.

A low risk of psychosis exacerbation following IV ketamine, according to Iosifescu, who is also the director of clinical research at the Kline Institute for Psychiatric Research in Orangeburg, New York, and was not involved in the study, is still possible given that the review is based on a small sample.

Veraart concurred, stating that “well-designed randomised controlled trials should be conducted to ascertain the efficacy, safety, and tolerability of ketamine in depressed individuals with a propensity to psychosis before administration on a large scale is pushed.”

The study received no particular funding. Outside of the submitted work, Veraart has received speaker honoraria from Janssen. Disclosures from the other authors are provided in the original publication. Iosifescu has advised clinics on the most effective ways to administer IV ketamine therapy as a consultant to the Centers of Psychiatric Excellence.

REFERENCES:

For Mental disease medications that have been suggested by doctors worldwide are available here https://mygenericpharmacy.com/index.php?cPath=77_478

Common Dry-Cleaning Agent May lead to Parkinson’s Disease

Common Dry-Cleaning Agent May lead to Parkinson’s Disease

Comments 0 Comment

Trichloroethylene (TCE), a chemical, has been linked by some researchers to Parkinson’s disease. Dry cleaning, degreasing, and even decaffeinating coffee have all been common uses for TCE.

According to recent study, the chemical’s capacity to reach the brain and harm cell mitochondria may be the root of the problem.

The authors claim that the chemical’s influence might be “enormous” given how commonplace it is in the environment. TCE should be outlawed, and people should be shielded from more exposure, as suggested alternatives.

According to the Parkinson’s Foundation, the substania nigra, a region of the brain that includes cells that create the neurotransmitter dopamine, is affected by Parkinson’s disease, a neurodegenerative condition.

Parkinson’s disease patients endure tremors, slowness of movement, limb stiffness, and balance issues.

Muhammed Ali and Michael J. Fox are two well-known public celebrities who suffer with the illness.

According to the authors, up to a third of the groundwater in the United States has TCE pollution. The chemical is additionally present in Camp Lejeune, a Marine Corps base, and 15 Superfund sites in Silicon Valley.

What is trichloroethylene (TCE)?

TCE is a chemical that is a colourless liquid that does not exist in nature. It is well known to smell like chloroform.

This substance can be found in a wide range of goods and businesses, such as:

  • industry-wide dry cleaning
  • metal scrubbing
  • wiping cloths
  • carpet and garment stain removers
  • lubricants
  • aerosol adhesives

Using TCE-containing products or working in a TCE-containing plant are two ways that people can be exposed to the chemical.

TCE can also contaminate our air, water, and food and drink by leaking into the soil, water, and air near where it is used or disposed of. High levels of TCE exposure can cause the following symptoms:

  • dizziness
  • headaches
  • confusion
  • nausea
  • facial paralysis

Link between TCE and Parkinson’s disease

According to the study, which was published in the Journal of Parkinson’s Disease, there may be a “invisible” cause of Parkinson’s disease that is related to the widespread use of TCE.

Dr. James Beck, Chief Scientific Officer of the Parkinson’s Foundation, commented on the study, saying, “We have known for some years that TCE exposure and Parkinson’s disease are related. I believe that this opinion piece effectively highlights the risks associated with TCE exposure.

The researchers’ findings are discussed in the study together with the evidence tying TCE to Parkinson’s disease.

TCE is lipophilic, as the scientists explain in their research, which means that it has a propensity to dissolve in fatty tissues. This makes it simple for it to enter the brain and other bodily tissues where it can wreck havoc with cell mitochondrial function. This sort of toxin is extremely toxic to dopamine-producing cells, which may help to explain how exposure to TCE might cause Parkinson’s disease.

Seven other people, including the late Senator Johnny Isakson, are also profiled. Isakson employed TCE to degrease aircraft during his time in the military; as a result, he eventually developed Parkinson’s disease as well as renal cell carcinoma, a cancer associated to TCE exposure.

The matter was initially brought to his notice, according to co-author Dr. Ray Dorsey, when his colleague, Dr. Caroline Tanner, told him about the exposures at Camp Lejeune.

TCE poses a “enormous” risk to the general public’s health, he claimed. “At one time, it was used by 10 million Americans, including printers, embalmers, mechanics, dry cleaners, chip manufacturers, engineers, painters, metal workers, pilots and others. It has been absorbed into the environment by millions more people.

Avoiding exposure to TCE

The issue of TCE contamination, according to Dorsey, requires a few actions. It must be prohibited first, along with tetrachloroethylene (PCE), another industrial solvent.

Second, home remediation systems such to those used for radon must be deployed to alert and protect persons who are at danger of exposure.

The connection between TCE and Parkinson’s disease, he added, has to be explored further through research. People can be exposed to TCE through contaminated soil, food, water, air, or direct skin contact, according to the U.S. Centers for Disease Control and Prevention.

You are most likely to become exposed by drinking polluted water, but you can also become exposed through the air as it is released from contaminated water, as a third of all groundwater may be affected.

Working in a sector where TCE is manufactured or utilised, like the degreasing business, is a significant additional method that you could be exposed to it. It can enter the body by coming into direct touch with the skin or by inhaling the vapours.

You may also be exposed through contaminated soil, such as that found in landfills. Moreover, TCE can enter your body through the consumption of contaminated foods or contact with consumer products that contain it.

According to the CDC, TCE is a common solvent used in a variety of products, including cold metal cleaners, adhesives, lubricants, paints, varnishes, paint strippers, and paints. Labels for these goods should include instructions on how to reduce exposure.

The Occupational Safety and Health Administration (OSHA) also mandates that your company give you a material safety data sheet (MSDS) outlining the dangers and proper handling techniques for any chemicals you use at work.

When exposed to TCE

A doctor can check for TCE in your blood, breath, or urine if you’ve recently been exposed to the substance, according to the Agency for Toxic Substances and Disease Registry (ATSDR).

It can also be tested for in the environment you have visited. But, once you’ve been exposed, there is no cure to get it out of your system. Either your breath will expel it or your kidneys will excrete it into your urine.

They advise avoiding any known toxic regions, such as those with tainted water, soil, or air.

You should always use items containing TCE in well-ventilated areas with the appropriate personal protective equipment, such as chemical-protection gloves, safety goggles, and respirators, in addition to adhering to any safety advice on such products.

High TCE exposure can, in the short term, irritate people and even make them pass out or become fatally ill. If you have been exposed to the chemical extensively, it is crucial to seek immediate medical care.

The individual should also be transferred to clean air, and any contaminated clothing should be taken off, if it’s safe to do so. If the skin or eyes have been exposed, thoroughly rinse them with water.

Kidney cancer and Parkinson’s disease have both been associated with long-term TCE exposure. The ATSDR advises that the greatest form of protection is to shield yourself from exposure altogether.

REFERENCES:

For more details, kindly visit below.

Explore the latest link between MS and Your Gut.

Explore the latest link between MS and Your Gut.

Comments 0 Comment

The central nervous system is impacted by the chronic disease known as multiple sclerosis (MS). When the immune system targets the outer layer of nerve cells, symptoms including weakness in the muscles and visual issues appear.

MS’s precise causation is unknown, however scientists believe that a number of variables may be involved. A recent study discovered that MS may be brought on in persons with a genetic predisposition by a toxin produced by a common gut bacterium.

Multiple sclerosis (MS) is a persistent nerve system disease. Young adults between the ages of 20 and 40 are the most frequently affected, and women are more likely than males to experience it.

There are around 2.8 million MS sufferers worldwide, and the number is growing, according to the Multiple Sclerosis International Federation (MSIF).

Symptoms of Multiple Sclerosis

The immune system of the affected person destroys the myelin sheath that protects the nerve fibers in this autoimmune illness. Sclerosis is a scar or lesion that results from damage. These lesions, which most frequently affect the central nervous system, can cause a variety of symptoms, such as:

Relapsing-remitting MS, the most prevalent type of MS that accounts for 85% of cases, is characterised by episodes of new or worsening symptoms and intervals during which symptoms subside or go away.

Scientists believe that environmental variables and genetic vulnerability may play a role in the development of the illness, while the specific reason is yet unknown. MS is riddled with many mysteries.

Epsilon toxin, which is produced by a bacteria that may be found in the small intestine, has now been linked to the development of MS and the maintenance of symptoms, according to study conducted by researchers at Weill Cornell Medicine’s Brain and Mind Research Center.

How the gut microbiota affects MS?

The trillions of bacteria that reside in your digestive system make up the gut microbiota. The majority of microbes are bacteria, but they can also include viruses, fungi, and the microscopic, single-celled creatures known as protozoa.

In general, these bacteria are beneficial and even essential to our health. Yet, dysbiosis, or an out-of-balance microbiota, can cause issues. According to studies, alterations in the microbiota may be a factor in various autoimmune diseases.

In MS patients, changes to the gut flora are frequent. According to this recent study, patients with MS are more likely than healthy controls to carry the pathogen Clostridium perfringens. Epsilon toxin, which is produced by C. perfringens, opens the blood arteries in the brain and permits inflammatory cells to enter the central nervous system (CNS).

What is the epsilon toxin?

Dr. Barbara Giesser stated that the researchers “investigated how the toxin induced an MS-like condition in a mouse model using unique and sensitive techniques to determine the presence of the bacterium.

The scientists collected faeces from both MS patients and healthy controls. They used polymerase chain reaction (PCR) analysis to examine these samples in order to find the epsilon toxin (ETX) gene, which is only present in C. perfringens.

They discovered that the ETX gene was present in 61% of samples from MS patients but only in 13% of those from healthy controls. Also, they discovered that compared to age- and sex-matched healthy controls, MS patients had a higher likelihood of having ETX-positive C. perfringens invade their gut microbiome.

Treatments to target this toxin

The current amount of knowledge regarding the gut microbiome in MS patients is expanded upon by this study. It has been demonstrated to respond to treatment with various disease-modifying treatments and is known to differ from those of non-MS controls, according to Dr. Barbara Giesser.

Epsilon toxin is only produced by C. perfringens during the rapid development phase. The researchers hypothesise that ETX is the cause of MS lesions, which would explain why the illness is episodic and manifests less symptoms when the toxin-producing bacteria are absent.

They draw the conclusion that the bacterium, its toxin, and MS exhibit a robust clinical connection. According to Dr. Giesser, this finding raises the prospect of therapies that target this pathway:

“The toxin facilitates central nervous system access for immune cells. This implies that medications that target the bacterium or the toxin may be effective in treating the condition.

The researchers point out that clinical trials would be required to see whether this could result in MS treatments.

Healthy microbiome

The development of MS may be significantly influenced by the gut microbiome, according to studies. An analysis of multiple research published in 2017 discovered that nutrition might be used to alter the gut flora and alter the course of MS.

The advantages of keeping a healthy gut microbiota are becoming more widely understood, and this study provides more proof that an unbalanced microbiota may lead to the onset of disease.

A healthy diet and lifestyle that promote the growth of advantageous gut flora may potentially lower the risk of MS as well as the risk of many other illnesses.

Improve gut health

Some elements, such as genetics and environment, are beyond your control. Although our gut microbiota is set up early in life, there are some things that can change it.

Certain modifications enhance the diversity and health of our microbiome. Alterations may be harmful.

These are some actions you may do to encourage a balanced, healthy gut microbiome:

  • Consume more fibre. All of the little microorganisms in your gut can eat fibre. Fruits, vegetables, beans, lentils, nuts, seeds, and whole grains all contain fibre.
  • Drink less alcohol. There is evidence that alcohol causes dysbiosis. You might want to think about reducing your drinking if you do.
  • Consume fermented food. Foods that have been fermented are sources of good bacteria and may be beneficial to health. Among the foods that are fermented include kimchi, tempeh, yoghurt, kefir, miso, and sauerkraut.
  • Stress management. Your gut microbiota’s state of health can be impacted by stress. To manage tension, try some stress-relieving exercises like yoga or meditation.
  • Don’t overuse antibiotics. Antibiotics can kill some of the helpful bacteria in addition to the harmful ones. Dysbiosis may result from this. Antibiotics should only be used as necessary, and they should be taken exactly as prescribed. Some of the beneficial bacteria may be restored by taking a probiotic supplement.
  • Look into probiotic dietary supplements. Supplements with probiotics may be beneficial. To determine the appropriate dosage and strain for particular ailments, more research is required. Start with the US Probiotic Guide if you want to.

Conclusive note

  • The human body is home to trillions of microorganisms. The gut contains the majority of them.
  • The possibility that the sorts of bacteria in our guts may have an impact on our health is intriguing.
  • Dysbiosis is more likely to occur in MS patients. When the gut microbiota is out of equilibrium, it is called dysbiosis. Inflammation and autoimmune illnesses are now more likely as a result.
  • A healthy gut microbiota can be supported by consuming fermented foods and a high-fiber diet.
  • There is continuing research into the potential benefits of altering the gut microbiome for MS patients.

REFERENCES:

For more details, kindly visit below.

How Bone Density May Be Linked to Dementia Risk?

How Bone Density May Be Linked to Dementia Risk?

Comments 0 Comment

According to researchers, a decline in bone density may be associated with a higher risk of dementia.

Low bone density and dementia tend to develop at later age, but the researchers caution that they are unsure of why there may be a connection.

A nutritious diet and regular exercise, according to experts, are two strategies to enhance overall bone health.

A study was published in Neurology, the official journal of the American Academy of Neurology. People with low bone density may be more likely to develop dementia. 3,651 individuals with an average age of 72 whose medical histories and X-rays were examined by Dutch researchers.

Everybody underwent physical exams, including X-rays and dementia screenings, as well as interviews every four to five years.

Prior to the trial, none of the subjects had dementia. Among the conclusions were:

  • Dementia affected 688 people (19%) over an average of 11 years.
  • 90 of the 1,211 individuals with the lowest bone density who lived the longest had dementia.
  • During a decade, 57 of the 1,211 individuals with the highest bone density had dementia.

The researchers found that those with lower bone density were 42% more likely to develop dementia than those with higher bone density. Even after controlling for age, sex, education, other illnesses, medicinal use, and family history of dementia.

The study only demonstrates a connection, not cause and effect, the researchers noted.

Bone density and dementia

According to the researchers, bone density loss may occur in the early stages of dementia and, if it does, may be a sign of risk.

With that information, healthcare providers may focus on providing earlier and more regular screenings. Also, a better care to those who have bone loss.

The researchers also stated that little was known about a potential connection in the years preceding dementia and that inactivity and poor nutrition. Both of which are present in dementia patients, both cause bone loss, which is accelerated by inactivity.

The majority of the individuals in the study were Europeans over the age of 70. They poses a drawback in that the findings may not be generalizable to other races, ethnicities, and age groups.

Dr. Joel Salinas, is a behavioural neurologist, researcher at NYU Langone Health and the chief medical officer at Isaac Health in New York. He stated that he always believes that additional research is necessary to determine why there may be a relationship.

According to Salinas, “In this scenario, there could be a few reasons why there is an association between dementia and bone loss.”

He listed a few potential explanations:

  • These two illnesses have a strong connection to ageing.
  • Both disorders may be influenced by inflammation in some way.
  • nutrition, diet, and way of life.

Salinas continued, “Improving lifestyle factors like nutrition and activity levels can never be too late. Even if there are already symptoms of cognitive deterioration, putting out a conscious effort in these areas can help prevent the progression of dementia.

Common Bed Partners

In the elderly population, Low bone mineral density (BMD) and dementia frequently co-occur, with bone loss accelerating in dementia patients as a result of inactivity and poor nutrition. It’s unknown, though, how much bone loss already exists before dementia manifests.

The new findings are based on 3651 seniors (mean age 72 years, 58% women). These were dementia-free between 2002 and 2005 and participated in the Rotterdam Study.

Dual-energy radiography absorptiometry (DXA) was used to measure BMD at the femoral neck, lumbar spine, and overall body at that time. The trabecular bone score, which provides additional information like bone microarchitecture, was also calculated. Up to January 1st, 2020, participants were monitored.

Age, sex, education, physical activity, smoking status, body mass index, blood pressure, cholesterol, history of comorbidities (stroke and diabetes), and apolipoprotein E genotype were all taken into account while doing the analyses.

In the 688 people who underwent follow-up who got dementia, the majority (77%), had Alzheimer’s disease.

Preventing bone loss

Dr. Nahid Rianon, a professor of general medicine at McGovern Medical School at UTHealth Houston who was not involved in the study, responded to Medical News Today when asked what would account for the connection between poor bone density and dementia risk:

Although this is a very useful study, it is impossible to determine if low bone density causes dementia, whether dementia causes low bone density, or whether low bone density and dementia share a risk factor.

The findings are significant because each of the three hypotheses has a critical role to play. To prevent both fatal diseases, it is imperative to find out if they share a common cause.

According to Rivadeneyra, “Dementia and bone health are two typical diseases we all struggle with to some extent as we age, so it’s no surprise there would be a correlation.” “We are aware that smoking increases the risk of dementia, low bone density, and cardiorespiratory problems. As we age, alcohol misuse is also linked to weak bones and dementia. Many of these ‘age-related’ diseases we frequently see are caused by heart disease, prolonged pharmaceutical usage (for some medications), injuries and trauma, metabolic issues like thyroid disease or diabetes, and a strong family history (genetics).

Consuming a diet high in calcium and vitamin D is also essential.

Osteoporosis and women

Osteoporosis is a prominent factor in broken bones in older men and postmenopausal women. Although each bone in the body has the potential to fracture, hip, vertebral, and wrist fractures are the most common in older people.

According to Dr. Gayatri Devi, a neurologist at Lenox Hill Hospital in New York, “women have a higher risk of osteoporosis and dementia, which could be related to decrease of oestrogen after menopause.”

According to Devi, those who engage in less physical activity—often older adults due to conditions like heart disease, diabetes, and stroke—have lower bone density and, thus, are at a greater risk for dementia.

The crucial conclusion, she continued, is that treating low bone density can lower the risk of dementia, fractures, and hospitalisation. “I think that everyone over the age of 50 should get a baseline bone density test because there is a good treatment, either through medication or exercise.”

Study limitations and implications

Dr. Wiggins noted that although other studies have described such relationships, since the majority of the patients in this study were in their 70s and of European heritage, they might not apply to other populations.

We must be careful not to conclude that lower bone density directly causes dementia, he cautioned, since this study merely found a link between bone and brain health.

Board-certified neuropsychologist Dr. Karen D. Sullivan, who runs the Pinehurst, North Carolina-based practise I CARE FOR YOUR BRAIN and was not engaged in the study, said:

The results of this study suggest that dementia may be more likely to strike those with inadequate bone density. According to Dr. Sullivan, this study “adds to the persuasive body of literature that demonstrates that maintaining bone health integrity is a crucial component of successful ageing.

“Evidence-based techniques for enhancing bone health after age 50 include putting a premium on high-quality animal/plant protein, polyunsaturated fatty acids, fruits and vegetables high in potassium, fibre, and foods high in calcium and vitamin D having the greatest study backing. In order to maintain strong, healthy bones as we age, frequent weight-loading and resistance exercises are also necessary, the expert concluded.

REFERENCES:

For more details, kindly visit below.

Focused ultrasound can improve Parkinson’s symptoms?

Focused ultrasound can improve Parkinson’s symptoms?

Comments 0 Comment

In a recent study, a novel, non-invasive method of using focused ultrasound to lessen Parkinson’s disease symptoms was presented. In order to disrupt the neural network that causes uncontrolled movement and motor dysfunction, the approach entails deleting a tiny neuron cluster.

Twice as many research participants received the new treatment than those who received sham care, and these improvements in symptoms frequently sustained for at least a year.

An innovative, noninvasive strategy for lowering dyskinesia, or uncontrollable movements, and motor impairment in Parkinson’s disease patients is presented in a recent study. Focused ultrasound is used in the novel technique.

When compared to trial participants who underwent a sham, or placebo, therapy, twice as many people reported improvement in dyskinesia and motor impairment three months after undergoing the incision-less procedure.

In 77% of individuals who responded to the medication, the gains persisted for up to a year. Patients who receive focused ultrasound therapy often return home the same day.

Gait issues, speaking difficulty, and eye disruption were among the infrequently reported negative effects by the researchers. The group that received the treatment experienced more severe adverse effects than the group that received a placebo.

Focused ultrasound

Focused ultrasound is a minimally invasive, non-surgical technique that causes an ablation in a region that reduces Parkinson’s and tremor symptoms. To produce a clear thermal lesion deep into the brain without harming nearby structures, we use focused ultrasonic waves. The basal ganglia are what we are primarily aiming for. A set of brain regions are involved in the coordination and control of movement. We employ a thermal imaging equipment for magnetic radiofrequency imaging (MRI) during the procedure. This gauges alterations in the skull’s temperature and enables us to guarantee the patient’s security.

The treatment is fantastic because it allows us to work on really delicate places securely, effectively, and with very minimal adverse effects.

Dopamine and L-DOPA

Parkinson’s disease is caused by low levels of the neurotransmitter dopamine in the substantia nigra of the brain. This is brought on by the death of neurons that produce dopamine.

The predominant idea holds that autophagy, the brain’s housekeeping mechanism, has failed, causing an accumulation of waste that impairs brain function.

Dopamine synchronises various brain regions so that they are communicating with one another at the same frequency, according to Dr. Jean-Philippe Langevin, director of the Pacific Neuroscience Institute’s Restorative Neurosurgery and Deep Brain Stimulation Program, who was not involved in the study.

“Consider all these parts of the brain as walkie-talkies or phones trying to communicate, but the frequency at which they’re trying to communicate is off,” said Dr. Langevin. Movements become stiff, hesitant, and tremble as a result, and are no longer flowing.

Dr. Langevin stated that the absence of dopamine causes the motor system of the brain, which regulates movement, to be “quite noisy.” Researchers can actually recognise electrical noise as this “noise.” According to recent research, Parkinson’s disease actually causes some neuronal frequencies to rise.

Levodopa, also known as L-DOPA, which replenishes dopamine in the brain, is the most widely used medication for the illness.

Yet, for many people, the dyskinesia and motor dysfunction they encounter are genuine side effects of L-DOPA therapy. Over time, the medication’s effectiveness deteriorates as well.

New treatment

The novel method examined in the trial is based on an essential tremor medication that was previously authorised in 2016.

A small group of neurons in the globus pallidus area of the brain are removed or ablate during focused ultrasound therapy. By leaving scarring on the tissue, ablation causes tissue destruction.

Dr. Howard M. Eisenberg, co-author of the study and professor of neurosurgery at the University of Maryland Medical System, with the following explanation of how a little more than 1,000 sound energy beams ablate the target tissue:

“Like light, sound can be concentrated. Imagine you had a magnifying glass when you were a child. If you focused the sun’s rays on a piece of paper, you would receive a tiny dot of light that would then transform into heat and burn a hole in the paper. With sound, we may achieve the same results.

When the beams are concentrated and the intensity is strong enough, “you can burn a little hole in the brain” precisely at the target location without harming surrounding tissue, he told us.

In essence, Dr. Eisenberg said, “that’s how it works: Back to the future, similar to ablation that was done years ago for essential tremor, but using different technology.”

According to Dr. Eisenberg, the dyskinesia and motor dysfunction are not always brought on by the ablated neurons. Instead, “it’s a system of targets that are interconnected nuclei, and you’re interrupting that system,” he said.

Motives for excitement

If the procedure enables Parkinson’s patients to take less L-DOPA medication, then there are many reasons to be optimistic, according to Dr. Langevin.

According to Dr. Eisenberg, based on prior experience with essential tremor ablation, we can anticipate benefits in roughly 80% of patients, and they might last at least five years.

However, not every participant in the research benefited from this treatment. A few participants, according to Dr. Eisenberg, might have skulls that are less effective at transmitting acoustic energy.

The reason for this is that the skull is made up of two hard layers of bone sandwiched by a softer layer, “like an Oreo biscuit,” rather than being one solid piece of bone.

Focused ultrasound vs. DBS

Dr. Eisenberg pointed out that deep brain stimulation is thought to be more successful for treating essential tremors than ablation (DBS). DBS stimulates tissue rather than destroying it. Furthermore, Parkinson’s dyskinesia and motor disability are treatable by DBS.

DBS, however, necessitates creating one or more tiny holes in the skull through which a wire is placed and directed to the desired location in the brain. The wire is then attached to a tiny neurostimulator that has been inserted into the chest.

“They won’t consider it even though we always explain that deep brain stimulation has advantages over focused ultrasound,” Dr. Eisenberg said of individuals who would prefer it instead. Hence, it’s beneficial for individuals who simply don’t want deep brain stimulation, which is understandable.

Yet, he added, the advantages provided by the new focused ultrasound approach are still potent enough to be life-altering.

REFERENCES:

For more details, kindly visit below.

Quick survey on Paralysis and its different types.

Quick survey on Paralysis and its different types.

Comments 0 Comment

What is Paralysis?

Loss of muscle function in the body is referred to as paralysis. Sometimes paralysis is transitory, and occasionally it is permanent. While paralysis can affect any portion of the body, the majority of cases are seen in the limbs. Paralysis, both partial and total, can happen at any time. There is no immediate pain experienced by a patient who is paralysed.

The treatment plan is designed to either cure or treat the condition, depending on the nature of the underlying cause, in order to prevent the patient’s everyday lifestyle from being significantly impacted.

The most frequent underlying cause of partial or total paralysis in a patient is a stroke. Incomplete paralysis means the patient has no control over the afflicted muscle tissue while partial paralysis means the patient still has some control over the affected muscle.

Types and causes of Paralysis

The paralysis types that are best known to the public are:

  • Monoplegia
  • Hemiplegia
  • Paraplegia
  • Quadriplegia
  • lock-in Syndrome

Monoplegia:

Monoplegia is a form of paralysis in which a person is unable to control one limb. The paralysis frequently affects just one arm, or occasionally only particular arm muscles. A common side effect of cerebral palsy is monoplegia. The brain’s capacity to control some body muscles is lost in cerebral palsy. The majority of cerebral palsy patients are young children and teenagers.

Since the patient can still do his everyday activities with only one limb paralysed, monoplegia is regarded as a positive indicator in the prognosis of this illness.

Hemiplegia:

Hemiplegia is a form of paralysis in which one side of the body loses control. This usually only has an impact on one arm or limb, though it might occasionally also have an impact on the torso. Hemiparesis is a condition in which a person’s functional use of their limbs is greatly diminished in terms of strength and endurance, but they retain some degree of functional use. In a few situations, hemiparesis progresses to hemiplegia.

When the corpus callosum between the left and right sides of the brain is damaged, hemiplegia can result. It can also result from spinal cord injury. A stroke, which impairs one side of the brain’s functionality, can also result in hemiplegia.

Left and right hemiplegia are additional divisions of hemiplegia. The diagnosis of right or left hemiplegia depends on where the injury is located.

Paraplegia:

In the case of paraplegia, the patient is unable to control their muscles below the waist. Each person experiences paraplegia differently. The fundamental cause of paraplegia typically arises in the brain or spinal cord, and people who experience it have completely normal legs. Sometimes a lower torso limb only has partial paraplegia, while other times it occurs completely. Regular physical therapy and medication are frequently responsible for partial paraplegia.

Paraplegia frequently results from a patient suffering from a brain, spinal cord, or both types of injuries. The impulses that the brain sends to the lower body are not returned to the brain through the spinal cord in paraplegic patients. Patients who suffer from this absence of brain communication not only lose their ability to move, but also their ability to feel.

A patient with partial or incomplete paraplegia may still be able to use one leg, whereas a patient with complete paraplegia loses sensation and use of both legs.

Quadriplegia

All four limbs of the body are paralysed in a quadriplegia. In this scenario, the patient’s hands and legs become impaled as a result of the brain’s signals to the areas below the neck not being returned. Sending and receiving signals from the brain is the responsibility of the spinal cord. This stops working in quadriplegia, resulting in the condition.

Quadriplegia may begin as a result of spinal cord or brain injuries. The likelihood of recovery from this condition increases as the wounds to the afflicted area heal or as the brain inflammation subsides. It is impossible to provide an accurate forecast, though.

In addition to exhaustion, sudden spasms, lack of sensation below the neck, trouble passing urine from the body, respiratory distress, bedsores, and depression, patients with quadriplegia also experience fatigue.

Locked-in Syndrome:

In a condition known as “Locked-in Syndrome,” the patient is unable to control any area of their body with their under-eye muscles. Locked-in syndrome is primarily a consequence of a serious brain damage, a stroke, or brain cancer. A person suffering from locked-in syndrome won’t be able to move any of his body’s limbs or his lips, jaw, or up and down or side to side movements in the neck. However, those who experience locked-in syndrome are still able to blink and move their eyes up and down.

Doctors rely on the moment of the eyes to make a precise diagnosis because locked-in syndrome frequently mimics the symptoms of a coma.

To ensure that the patient gets all the nutrients needed, adequate nutrition is essential. However, the patient must be fed through a stomach tube, which must either be inserted directly into the stomach through an incision made in the small intestines or through the nose.

Patients who spend a lot of time in bed can develop pressure sores, blood clots, damaged muscles, and damaged nerves. By moving the patient, rubbing the muscles, rotating the joints along their axes, and using physiotherapy, care should be given to prevent pressure sores.

Complications of paralysis

Other physiological processes including respiration and heart rate might be impacted by paralysis. Other body systems in the affected area may also be affected by the illness. Depending on the kind of paralysis you have, you could be vulnerable to:

  • breathing issues, coughing, and pneumonia risk.
  • Deep vein thrombosis (DVT) and clots in the blood.
  • issues with speech or swallowing (dysphagia).
  • both anxiety and depression.
  • Sexual difficulties and erectile dysfunction.
  • Excessively high blood pressure (autonomic dysreflexia) or low blood pressure (orthostatic hypotension) and heart problems.
  • bowel incontinence and urinary incontinence.
  • Sepsis and pressure wounds (bedsores).

How is paralysis diagnosed?

Paralysis is frequently simple to diagnose, particularly when your lack of muscle function is visible. Your doctor may employ X-rays, CT scans, MRI scans, or other imaging techniques to examine inside body parts where paralysis is more challenging to detect.

If you suffer a spinal cord injury, your doctor might perform a myelogram to determine how you are doing. In this surgery, a particular dye will be injected into the spinal cord’s nerves. This will make it easier for them to see your nerves on X-rays. In addition, they might conduct an electromyography. They will utilise sensors to assess the electrical activity of your muscles during this operation.

How is paralysis treated?

The underlying cause of the paralysis as well as the symptoms present will determine a therapy strategy. For illustration, a physician would advise:

  • operation or potential amputation
  • physical exercise
  • Workplace therapy
  • wheelchairs, braces, portable scooters, and other mobility aids
  • If you have spastic paralysis, you may take drugs like Botox or muscle relaxants.

Paralysis is frequently incurable. However, a medical team might suggest a range of medications, equipment, and tactics to assist manage symptoms.

REFERENCES:

For more details, kindly visit below.

Contrasting types of Brain aneurysm and their symptoms.

Contrasting types of Brain aneurysm and their symptoms.

Comments 0 Comment

An aneurysm is an artery that has enlarged due to weakened arterial wall. Even though an aneurysm rupture can result in catastrophic complications, it frequently has no symptoms. An aneurysm is a bulge or distention of the artery caused by a weakening of the artery wall.

The majority of aneurysms are not harmful and exhibit no symptoms. Some, however, have the potential to burst at their most serious state, resulting in potentially fatal internal haemorrhage.

Over 25,000 deaths in the United States (U.S.) are attributed to aortic aneurysms each year, according to the Centers for Disease Control and Prevention (CDC). Every year, some 30,000 brain aneurysms burst in the United States. About 40% of these cases result in death within 24 hours.

What is Brain aneurysm?

A brain aneurysm is a condition of the artery in which a region of the arterial wall bulges and swells with blood. It can also be referred to as a cerebral or intracranial aneurysm.

Any age can be affected by a brain aneurysm, which has the potential to be fatal. If a brain aneurysm ruptures, it is a medical emergency that, if left untreated, might result in a stroke, brain damage, and even death.

Types of Brain aneurysm

The location of an aneurysm within the body determines its classification. The two most typical locations for a severe aneurysm are the heart’s arteries and the brain’s arteries.

There are two primary shapes for the bulge:

  • Blood vessels with fusiform aneurysms bulge on all sides.
  • Saccular aneurysms only have a side that bulges.

The size of the bulge affects the chance of rupture.

Aortic aneurysm

The left ventricle of the heart is where the aorta originates. It then travels through the chest and abdominal cavities. The aorta’s diameter is from 2 to 3 centimetres (cm), but an aneurysm can cause it to swell to more than 5 cm.

Abdominal aortic aneurysms are the most prevalent aortic aneurysms (AAA). The area of the aorta that passes through the abdomen is where this happens. The annual survival rate for a AAA larger than 6 cm is 20% without surgery.

AAA can quickly turn fatal, but those who make it to the hospital have a 50% chance of surviving the rest of their lives.

Less frequently, the portion of the aorta that runs across the chest may be affected by a thoracic aortic aneurysm (TAA). Without treatment, TAA has a survival probability of 56% and an overall recovery rate of 85% after surgery. As only 25% of aortic aneurysms form in the chest, it is a rare disorder.

Cerebral aneurysm

Intracranial aneurysms are aneurysms in the blood vessels that supply the brain. They are frequently referred to as “cherry” aneurysms due to their appearance.

Within 24 hours, a brain aneurysm rupture can be fatal. Around 66 percent of people who survive brain aneurysms will have a neurological impairment or disability as a result. Brain aneurysms account for 40% of fatalities.

The most frequent cause of a form of stroke known as subarachnoid haemorrhage is ruptured brain aneurysms (SAH).

Peripheral aneurysm

An aneurysm in the popliteal region develops behind the knee. The most frequent peripheral aneurysm is this one.

  • Aneurysm of the splenic artery: This kind develops close to the spleen.
  • Splenic artery aneurysm: This type of aneurysm occurs near the spleen.
  • Mesenteric artery aneurysm: The artery that carries blood to the intestines is impacted by this.
  • Femoral artery aneurysm: The femoral artery is located in the groyne and can rupture.
  • Carotid artery aneurysm: This happens in the neck.
  • Visceral aneurysm: Aneurysm of the arteries supplying blood to the gut or kidneys is known as a visceral aneurysm.

Aortic aneurysms are more prone to burst than peripheral aneurysms.

Symptoms of Brain aneurysm

Unless it ruptures, a brain aneurysm rarely exhibits any symptoms (ruptures). If a brain aneurysm is unusually large or presses against brain tissues or nerves, it may occasionally induce symptoms even if it is unruptured.

Unruptured brain aneurysm symptoms can include:

If you have signs of a brain aneurysm that has not ruptured, you should visit a doctor as soon as possible. Although aneurysms typically do not burst, it is always crucial to have one evaluated in case medical attention is required.

An intense headache that strikes out of nowhere is typically the first sign of a ruptured brain aneurysm. It has been compared to getting hit on the head and causes blinding anguish unlike anything else ever felt.

Other signs of a ruptured brain aneurysm may also manifest suddenly and include the following:

  • an ill feeling or being
  • a sore neck or ache in the neck
  • responsiveness to light
  • double or blurry vision
  • abrupt confusion
  • consciousness is lost
  • fits (seizures)
  • weakness in any limbs or on one side of the body

Causes of Brain aneurysm

An artery in the brain experiences structural alterations that lead to brain aneurysms. The artery’s walls weaken and thin as a result of these alterations. The distortion may result from wall weakening, but it is also possible for inflammation or trauma to be the only cause of the deformity.

What specifically causes aneurysms to occur is still a mystery. But it’s thought that one or a few of the following elements might favour their development:

  • an elastic tissue breakdown inside the artery
  • stress brought on by the artery’s blood flow
  • because of an increase in inflammation, the artery’s tissue has changed.

Additionally, where an artery splits off into several directions, brain aneurysms are more likely to occur. This is due to the weaker arteries that are present there by nature.

Aneurysms can develop at any time after birth. But they typically come about throughout the course of your lifetime.

Complications of Brain aneurysm

Complications from a ruptured aneurysm could be one of its early warning indications. Instead of only the aneurysm, a rupture is more likely to cause symptoms.

The majority of persons who have an aneurysm do not have any complications. However, problems can also include the following in addition to thromboembolism and aortic rupture:

  • Severe chest or back pain: After an aortic aneurysm in the chest ruptures, severe chest or back pain may develop.
  • Angina: Another form of chest pain that can result from some aneurysms is angina. Myocardial ischemia and heart attacks can result from angina.
  • A sudden extreme headache: An unexpectedly strong headache is the primary sign of SAH caused by a brain aneurysm.

Any aneurysm rupture may result in pain, low blood pressure, a fast heartbeat, and dizziness. The majority of persons with an aneurysm won’t have any problems.

Prevention of Brain aneurysm

Since certain aneurysms are congenital—that is, existing from birth—it is not always possible to prevent them. But some lifestyle decisions can influence the risk:

  • Smoking increases the risk of developing aortic aneurysms and having an aneurysm rupture in any part of the body. Smoking cessation can lower the risk of developing a serious aneurysm.
  • Reduced aneurysm risk can also be achieved by controlling blood pressure. Dietary changes, regular exercise, and medication can all help lower blood pressure to a healthy level.
  • These actions are crucial for lowering pressure on the arterial walls since obesity can put the heart under additional strain.
  • Additionally, a healthy diet helps lower cholesterol and lower the risk of atherosclerosis. Atherosclerosis and fusiform aneurysms frequently go hand in hand.

Anyone who has been given a conservative treatment plan after being diagnosed with an aneurysm can work with a medical professional to address any risk factors.

REFERENCES:

For more details, kindly visit below.

Important note on Parkinson’s disease you need to know.

Important note on Parkinson’s disease you need to know.

Comments 1 comment

Parkinson’s disease is a neurological condition that worsens over time. Movement issues are one of the earliest symptoms. Dopamine is a chemical that exists in the brain and is responsible for smooth and coordinated motions of the body’s muscles. The “substantia nigra” is a region of the brain where dopamine is made.

The substantia nigra cells begin to deteriorate in Parkinson’s disease. Dopamine levels drop as a result of this. Parkinson’s disease symptoms begin to show up when they have decreased by 60 to 80%.

Parkinson’s disease stages

Parkinson’s is a progressive illness, which means that over time, the condition’s symptoms usually get worse.

The Hoehn and Yahr scale is frequently used by doctors to categorise its stages. This scale categorises symptoms into five phases and aids medical practitioners in determining the severity of disease symptoms and signs.

Stage 1

Stage 1 is the mildest type is Parkinson’s. In fact, it’s so mild that you could not even notice any symptoms. Your regular activities and chores might not yet be affected by them.

Even if you do experience symptoms, they might just affect one side of your body.

Stage 2

It may take months or even years for stage 1 to move into stage 2. The experiences of each person will vary. You might feel symptoms at this stage, which is moderate such as:

Stiffness in your muscles can make regular tasks more difficult and take longer to complete. However, you probably won’t have any balance issues at this point.

The body’s two sides may experience the same symptoms. Posture, movement, and facial expression modifications may be more obvious.

Stage 3

The symptoms change course at this midpoint. You probably won’t develop any new symptoms, but they might become more obvious. They might also obstruct all of your daily activities.

Activities move more slowly as a result of the noticeable slower movements. Falls can grow more frequent as balance problems become more serious. However, people with Parkinson’s disease in stage 3 can typically keep their independence and carry out daily tasks without much help.

Stage 4

There are substantial modifications as the stages 3 and 4 proceed. Without a walker or other aid, it will be quite difficult for you to stand at this point.

Significantly slower reactions and muscle motions are also observed. It might be risky and unsafe to live alone.

Stage 5

In this most advanced stage, constant help is required due to the intense symptoms. Standing will be challenging, if not impossible. Most likely, a wheelchair will be needed.

Parkinson’s patients may also have disorientation, delusions, and hallucinations at this stage. The disease’s consequences can start developing in its latter stages.

Symptoms of Parkinson’s disease

Some of the early signs of Parkinson’s can show up years before there are any movement issues. These initial indications include:

  • reduced capacity to smell (anosmia)
  • constipation
  • tiny, squished handwriting
  • voice variations
  • hunched position

The four most prevalent motor issues include:

  • tremor (shaking that occurs at rest)
  • sluggish motions
  • rigidity in the arms, legs, and trunk
  • difficulties with balance and a propensity to tumble

Additional signs include:

  • blank look on the face
  • a propensity to become trapped while walking
  • low-pitched, muted speech
  • reduced swallowing and blinking
  • inclination to reverse direction
  • shortened arm walking while swinging
  • Parkinsonian gait, or the propensity to walk with shuffled steps

Additional signs and symptoms could be:

  • Seborrheic dermatitis is the condition when the skin develops flaky white or yellow scales on greasy areas.
  • greater likelihood of developing the deadly skin disease melanoma
  • vivid dreams, chatting, and movement while sleeping are all signs of disturbed sleep.
  • depression
  • anxiety
  • hallucinations
  • psychosis
  • issues with focus and memory
  • visual-spatial interactions are challenging

Parkinson’s disease’s early warning signals could go unnoticed. With these warning signals, your body may try to warn you of the movement issue years before any movement difficulties appear.

Causes of Parkinson’s disease

Parkinson’s disease is a neurological condition brought on by alterations in the brain. Although the exact reason why it occurs is unknown, scientists have found some varieties that do.

Low dopamine levels

Parkinson’s disease symptoms are mostly brought on by low or declining levels of the neurotransmitter dopamine. It occurs when brain cells that make dopamine die.

The area of the brain that regulates movement and coordination receives information from dopamine. Therefore, it may be more difficult for people to control their movement when dopamine levels are low.

The severity of the symptoms gradually worsens as dopamine levels continue to drop.

low levels of norepinephrine

Damage to the nerve terminals that create another neurotransmitter, norepinephrine, which supports blood circulation and other natural bodily activities, may also be a component of Parkinson’s disease.

Parkinson’s disease patients with low norepinephrine levels may have both motor and nonmotor symptoms like:

  • rigidity and stiffness
  • physical unsteadiness
  • tremor
  • anxiety
  • having trouble focusing
  • dementia
  • depression

This may help to explain why orthostatic hypotension frequently occurs in persons with Parkinson’s disease. When someone stands up, their blood pressure fluctuations, which can cause dizziness and a chance of falling, is referred to as this.

The Lewy body

The brain of a person with Parkinson’s disease may have Lewy bodies, or clusters of the protein alpha-synuclein. Changes in movement, thinking, behaviour, and mood can result from the buildup of Lewy bodies, which can also result in nerve cell death. Dementia may also result from it.

Lewy body dementia is not the same as Parkinson’s disease, although because the symptoms are similar, some people may have both.

Genetic factors

Although mutations in numerous genes have been found to be associated with Parkinson’s disease, experts do not believe this to be a hereditary ailment.

Only 10% of cases, particularly in those with early-onset disease, seem to be genetic in nature.

Autoimmune factors

According to a 2017 study, there may be a hereditary connection between inflammatory diseases like rheumatoid arthritis and Parkinson’s disease.

In 2018, Taiwanese health data were examined by researchers who discovered a 1.37-fold increased risk of Parkinson’s disease in patients with autoimmune rheumatic disorders.

Risk factors for parkinson’s disease

Parkinson’s disease risk may be increased by a number of environmental variables.

These consist of:

  • Past traumatic brain injury: For instance, head traumas sustained while playing contact sports may raise the likelihood of the illness.
  • Exposure to toxins: These include metals, pesticides, solvents, and other contaminants.
  • Males are 50% more likely than females to have the illness, while a 2016 study found that the risk for females may rise with age.
  • Age: The illness frequently manifests around the age of 60.
  • Some pharmaceuticals: Some drugs can cause Parkinsonism, a condition in which a person exhibits tremors and other symptoms but does not have Parkinson’s disease.

Symptoms typically start to show up around the age of 60. However, early-onset Parkinson’s, which manifests before the age of 50, affects 5–10% of those who have the condition.

Statistics in the past have indicated that Black Americans are less likely than people of other ethnicities to have Parkinson’s disease.

The lack of knowledge about how the disease can affect Black people and a higher likelihood of misdiagnosis as a result of unequal access to healthcare, according to experts, may be to blame for this.

REFERENCES:

  • https://www.healthline.com/health/parkinsons
  • https://www.medicalnewstoday.com/articles/323409
  • https://www.mayoclinic.org/diseases-conditions/parkinsons-disease/symptoms-causes/syc-20376055
  • https://my.clevelandclinic.org/health/diseases/8525-parkinsons-disease-an-overview
  • https://www.nia.nih.gov/health/parkinsons-disease

For more details, kindly visit below.

Important note on causes and treatment for brain cancer.

Important note on causes and treatment for brain cancer.

Comments 0 Comment

The development of malignant cells in the brain leads to brain cancer. Depending on the type of tumour, the cancer cells produce slow- or fast-growing tumours.

The goal of brain cancer treatment is to remove the tumour and then eradicate any cancer cells that may still be present. In particular for slow-growing tumours, new advancements in brain cancer therapies are increasing survival rates.

What is brain cancer?

Primary brain cancer, commonly referred to as brain cancer, is characterised by an excess of brain cells that develops into masses known as brain tumours. Cancer, on the other hand, begins in another place of the body and progresses to the brain. It is referred to as secondary or metastasized brain cancer when that occurs.

Some malignant brain tumours have a rapid rate of growth. These cancerous tumours may interfere with how your body functions. Brain tumours should be treated as soon as they are discovered since they can be fatal.

Brain tumours are rather rare. People have a less than 1% lifetime chance of getting a malignant brain tumour, according to estimates from the American Cancer Society.

Types of brain tumors

Names for brain tumours are determined by their location within the brain or upper spine. A grade is also assigned to tumours. You can determine the projected rate of growth of a tumour by looking at its grade. Grades range from one to four, with four being the fastest-growing grades and one being the slowest.

The following are some of the most prevalent kinds of brain tumours:

  • Glioma. About 3 out of 10 occurrences of brain cancer are gliomas, which are brain tumours that start in the glial cells.
  • Astrocytoma. Glioblastomas, the kind of quickly-expanding brain tumour, are a subtype of astrocytomas.
  • Meningioma. Meningioma tumours, the most prevalent kind of brain tumour in adults, develop in the tissue that surrounds your brain and spinal cord and are frequently benign and slow-growing.
  • Ganglioglioma. Surgery is typically used to treat the slow-growing tumours known as gangliogliomas that are present in glial and neuronal cells.
  • Craniopharyngiomas. Craniopharyngiomas are slow-growing tumours that develop between the pituitary gland and the brain. Because they frequently encroach on the optic nerves, they can impair eyesight.
  • Schwannomas. Almost typically benign, schwannomas are slow-growing tumours that develop around the cranial nerves.
  • Medulloblastoma. Children are more likely to develop medulloblastomas, which are rapidly developing tumours that develop on the nerve cells in the brain.

Symptoms of brain cancer

The size and location of the brain tumour affect the symptoms of brain cancer. Particularly in its early stages, brain cancer exhibits many of the same symptoms as a number of less dangerous diseases.

Numerous of these symptoms are extremely typical and are not likely to be signs of brain cancer. However, it’s a good idea to see a doctor if you’ve had any of these symptoms for longer than a week, if they came on suddenly, if they don’t go away with over-the-counter painkillers, or if any of them worry you.

Typical signs of brain cancer include:

  • morning headaches that are typically worse
  • nausea
  • vomiting
  • a miscommunication
  • a loss of equilibrium
  • having trouble walking
  • Memory problems
  • having trouble thinking
  • speech issues
  • vision issues
  • personality alters
  • inconsistent eye motions
  • body jerking
  • muscle jerking
  • unexpected fainting or syncope
  • drowsiness
  • tingling or numbness in the arms or legs
  • seizures

Early diagnosis significantly improves the prognosis for brain cancer. If you frequently suffer any of the aforementioned symptoms or suspect that your symptoms may be more serious, schedule an appointment with a doctor right away for a diagnosis.

Causes and risk factors

Primary brain cancer has an unidentified specific cause. However, studies have connected excessive ionising radiation exposure to a higher chance of developing brain cancer. The most frequent sources of ionising radiation include radiation therapy treatments, frequent medical imaging tests (CT scans and X-rays), and potential employment exposure.

Additional factors that could increase the risk of acquiring brain cancer include:

  • greater age
  • a history of brain cancer in the family
  • chronic smoking
  • being exposed to fertilisers, pesticides, and herbicides
  • working with substances like lead, plastic, rubber, petroleum, and some textiles that might cause cancer
  • having mononucleosis or Epstein-Barr virus infection

Secondary brain cancer Some types of cancer are more likely than others to cause brain cancer, which develops when cancer that started in another part of your body travels to your brain.

The following cancers frequently metastasis, or spread, to the brain:

  • lung disease
  • mammary cancer
  • renal cancer
  • urethral cancer
  • melanoma, a form of skin cancer

How is brain cancer treated?

Brain cancer can be treated in a number of ways. A primary brain cancer will be treated differently than a cancer that has spread to other organs.

The kind, size, and location of your brain tumour will determine whether you receive one therapy or more. There will also be considerations for your age and general health.

Treatments for brain tumours include:

Surgery.

The most frequent form of treatment for brain tumours is brain surgery. Depending on the tumor’s position, it might be possible to remove it whole, partially, or not at all.

Chemotherapy.

These medications can reduce your tumour and kill brain cancer cells. Chemotherapy can be administered orally or intravenously.

Radiation treatment. 

Using high-energy waves like X-rays, this procedure eliminates cancer cells and tumour tissue that can’t be removed surgically.

Combination treatment.

Combination therapy refers to the simultaneous administration of chemotherapy and radiation therapy.

Biologic medicines

These medications support, guide, or restore your body’s natural tumour defences. For instance, immunotherapy is a class of biologic medication that is frequently prescribed and increases your immune system’s capacity to recognise and combat cancer.

Other medicines.

To treat symptoms and adverse effects brought on by your brain tumour and brain cancer therapies, your doctor may prescribe drugs.

Clinical studies.

Clinical trial medicines and drugs may be employed in advanced brain cancer instances that don’t respond to treatment. These are medications that are still being tested. An immunotherapy trial and a CAR T cell therapy trial may be part of clinical trials for brain cancer.

Rehabilitation.

If your disease or treatment have made it difficult for you to speak, walk, or perform other daily tasks, you might need to go to rehabilitation sessions. Physical therapy, occupational therapy, and other types of therapies are all included in rehabilitation. These treatments can assist you in relearnng activities.

Various forms of treatment.

There isn’t much evidence to back up the use of complementary medicines to treat brain cancer. To make up for the nutrients lost during cancer treatment, some medical specialists do advise taking measures like following a bland diet and taking vitamin and mineral supplements. 

Before making any dietary changes, using any herbs or supplements, or pursuing any alternative treatments, see your doctor.

How to reduce your risk of brain cancer?

Although there is no known way to prevent brain cancer, you can lower your risk by staying away from:

  • pesticide and insecticide exposure
  • exposure to cancer-causing substances
  • smoking
  • radiation exposure that is not essential

REFERENCES:

  • https://www.healthline.com/health/brain-cancer
  • https://www.cancercenter.com/cancer-types/brain-cancer
  • https://www.mayoclinic.org/diseases-conditions/brain-tumor/symptoms-causes/syc-20350084

For more details, kindly visit below.