Brain Mysteries

Dizziness after getting up may indicate a serious health problem

Frequent feelings of dizziness several minutes after getting up may signal an underlying health problem, according to new research published in Neurology.

On getting up, a sudden drop in blood pressure may lead to dizziness, lightheadedness or even blurred vision, though it could simply be due to dehydration or medication.

However, if it happens often, it could be an indicator of something more serious taking place called orthostatic hypotension (OH), according to new research undertaken by a team at the Harvard Medical School in Boston, MA.

OH is the lowering of blood pressure after changing position. This might occur within 3 minutes of getting up or sitting down.

The research team looked at the medical records of 165 people who had undergone nervous system testing – a test undertaken to see whether the autonomic nervous system is functioning normally.

54% of people with delayed OH progressed to full OH

Of these individuals, 48 had been diagnosed with delayed orthostatic hypotension (DOH), 42 had been diagnosed with OH – a more serious form of DOH – while 75 had neither condition. The average age of participants was 59.

During the 10-year follow-up period, 54% of individuals with DOH progressed to OH, while 31% developed a degenerative brain disease, such as Parkinson’s disease or dementia with Lewy bodies – disease caused by abnormal protein accumulation in the brain. Those with DOH who also had diabetes at study baseline were more likely to develop the full condition than those without diabetes.

The rate of death among study subjects was 29% for those with DOH and 64% for those with OH. For those with neither condition, the death rate was 9%.

For subjects with DOH who progressed to OH, the death rate over 10 years was 50%.

Many of those with DOH who did not develop the full condition were taking medication that may have affected their blood pressure, according to the researchers.

Commenting on the results, study author Dr. Christopher Gibbons, of Harvard Medical School, says:

“Our findings suggest that more than half of people with the delayed form of this condition will go on to develop the more serious form of this disease,” says study author l.

Our findings may lead to earlier recognition, diagnosis and treatments of this condition and possibly other underlying diseases that may contribute to early death.”

The researchers say there are limitations to the study. For example, because it was a retrospective review of previously collected data and all participants were referred to a specialized center for nervous system tests, the findings may not apply to the general population.

Source: mnt

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Link found between brain activity, empathy and borderline personality disorder

Recent data support the heterogeneity of borderline personality disorder and suggest that reduced brain activity may affect empathic processing among individuals with the disorder.

To assess associations between brain activity and empathy among individuals with borderline personality disorder, Brian W. Haas, PhD, and Joshua Miller, PhD, of the University of Georgia, conducted functional MRI while study participants completed an empathetic processing task in which they matched the emotion of faces to a situation’s context. Researchers included geometric shapes in place of emotional faces as a control. Participants (n = 82) completed the Five Factor Borderline Inventory to determine the severity of various traits associated with borderline personality disorder.

“Our results showed that people with [borderline personality disorder] traits had reduced activity in brain regions that support empathy,” Haas said in a press release. “This reduced activation may suggest that people with more [borderline personality disorder] traits have a more difficult time understanding and/or predicting how others feel, at least compared to individuals with fewer [borderline personality disorder] traits.”

Higher borderline personality disorder trait scores were associated with hypoactivity in two brain regions associated with cognitive empathy: the superior temporal sulcus and the temporoparietal junction.

“We found that for those with more [borderline personality disorder] traits, these empathetic processes aren’t as easily activated,” Miller said in the press release. “Borderline personality disorder is considered one of the most severe and troubling personality disorders, [and] can make it difficult to have successful friendships and romantic relationships. These findings could help explain why that is.”

Source: healio

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New study finds brain disease in 95% of deceased NFL players

The new football season is well underway, and with it comes the longstanding debate about the role football plays in long-term brain disease. Now, researchers report having found evidence of brain disease in 95% of brains tested belonging to former NFL players.

Researchers with the Department of Veterans Affairs and Boston University, MA, identified chronic traumatic encephalopathy (CTE) in 87 of 91 deceased NFL players, indicating that there is a link between football and long-term brain disease.

The findings were first reported by PBS and published on the website of the Concussion Legacy Foundation, whose brain bank received a $1 million research grant from the NFL in 2010.

“People think that we’re blowing this out of proportion, that this is a very rare disease and that we’re sensationalizing it,” says Dr. Ann McKee, chief of neuropathology at the Department of Veterans Affairs Boston Healthcare System. “My response is that where I sit, this is a very real disease. We have had no problem identifying it in hundreds of players.”

The team has previously identified CTE in the brains of football players who have donated their brains to science. So far, they have identified CTE in 96% of NFL players and 79% of football players examined to date – a total of 131 out of 165 individuals.

CTE occurs when an individual receives blows to the head over a period of time, causing progressive damage to nerve cells in the brain. The condition can impair cognitive functioning, causing difficulties with thinking and emotions and leading to problems such as depression and dementia.

The injuries that result in CTE cause the abnormal accumulation of proteins, interference in cell-to-cell communication and alter the white matter in the brain.

Previous research has suggested that repetitive minor head trauma represents a bigger risk to players than rare but violent collisions. The researchers found that 40% of the footballers who had CTE had played as offensive and defensive linemen – positions that experience physical contact on every play of a game – supporting past studies.

Findings ‘remarkably consistent’ with previous studies

This research is not the first to put football under increased scrutiny concerning the health and welfare of its players. Earlier this year, Medical News Today reported on a study published in JAMA Neurology that found retired NFL players with a history of concussion were at an increased risk for brain shrinkage and memory problems.

A number of former NFL players have taken legal action against the league on account of injuries and related health problems they have developed in later life associated with the sport, conditions that include dementia andamyotrophic lateral sclerosis (ALS). In April, a $1 billion settlement with around 5,000 former players was approved.

The NFL gave the following statement in response to the findings:

“We are dedicated to making football safer and continue to take steps to protect players, including rule changes, advanced sideline technology, and expanded medical resources. We continue to make significant investments in independent research through our gifts to Boston University, the [National Institutes of Health] and other efforts to accelerate the science and understanding of these issues.”

CTE can only be fully diagnosed after death. Many of the former footballers who had donated their brains to research had concerns about possible neurological problems while alive. This potential selection bias means that the researchers cannot guarantee the population they have analyzed is representative of all footballers.

To determine the overall incidence of CTE among footballers, the researchers will need to analyze the brains of a number of players who had never exhibited any signs or symptoms of the disease.

Despite this potential limitation, Dr. McKee states that their figures are “remarkably consistent” with previous research. She told PBS that the biggest challenge that now remains is convincing people with a vested interest in football that CTE is “an actual disease.”

“People want to make this just Alzheimer’s disease or aging and not really a disease,” she says. “I think there’s fewer of those people, but that’s still one of our major hurdles.”

Source: Medical News Today

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Brain-computer link enables paralyzed California man to walk

A brain-to-computer technology that can translate thoughts into leg movements has enabled a man paralyzed from the waist down by a spinal cord injury to become the first such patient to walk without the use of robotics, doctors in Southern California reported on Wednesday.

The slow, halting first steps of the 28-year-old paraplegic were documented in a preliminary study published in the British-based Journal of NeuroEngineering and Rehabilitation, along with a YouTube video.

The feat was accomplished using a system allowing the brain to bypass the injured spinal cord and instead send messages through a computer algorithm to electrodes placed around the patient’s knees to trigger controlled leg muscle movements.

Researchers at the University of California, Irvine, say the outcome marks a promising but incremental achievement in the development of brain-computer interfaces that may one day help stroke and spinal injury victims regain some mobility.

Dr. An Do, a study co-author, said clinical applications were many years away. Results of the UC Irvine research still need to be replicated in other patients and greatly refined.

Nevertheless, the study proved it possible “to restore intuitive, brain-controlled walking after a complete spinal cord injury,” said biomedical engineer Zoran Nenadic, who led the research.

The steps taken a year ago by the experiment’s subject, former graduate student Adam Fritz, who injured his back in a motorcycle accident, appear modest as seen in the video.

Fritz propelled himself over a distance of 3.6 meters (11.8 feet) across the floor of UC Irvine’s iMove Lab, though his weight was partially supported by an overhead suspension harness and a walker he grasped to keep his body upright, researchers said.

The weight support was necessary because the patient lacked any sensation in his legs or feet, Do explained.

Still, the experiment built on earlier UC Irvine studies in which brain signals were transmitted to a robotic prosthesis attached to the patient’s legs to produce movement, Do said.

In previous research by other scientists, a brain-computer interface has been used to allow paralyzed patients to grasp a cup of coffee with a robotic arm and raise the beverage to their mouths.

The latest study, which began about five years after Fritz became paralyzed, involved months of mental training in which he practiced thinking about walking to produce necessary leg-moving brain waves.

Those signals were then picked up by an electroencephalogram (EEG) he wore as a cap and were transmitted to a computer for processing by a special algorithm that could isolate the messages related only to leg motion and convert them to signals that would stimulate the patient’s muscles to walk.

The scientists and patient first practiced with a virtual-reality-like video game in which Fritz was trained to control a walking avatar. He also underwent extensive physical rehab to strengthen his muscles.

Fritz next practiced walking in the actual lab while suspended slightly above the floor. On his 20th outing, he finally took his first real steps on the ground.

Researchers hope to refine the technology by miniaturizing the EEG component enough to be implanted inside the patient’s skull or brain, allowing for clearer reception of the neural messages and perhaps the delivery of pressure sensation from sensors in the foot back to the brain.

Source: Reuters

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Timaru 8-year-old's brain tumours down to genetic disorder

Grace Hooke had perfect handwriting before she broke her arm.

It was an awkward fracture, about this time last year, right near the elbow.

When the Timaru 8-year-old’s perfect control of her pen started to deteriorate, her parents, Roger and Tracy Hooke, put it down to the break.

By that point, the usually bubbly Grace had started to become moody. “Haywire” is the term Tracy used to describe the way her only child’s brain was acting.

A different Grace from the one they were used to, one who never listened and was frequently in trouble at Grantlea Downs school, began to emerge.

After visits to the Child and Adolescent Mental Health Service at Timaru Hospital, Grace was given ritalin for attention deficit hyperactivity disorder (ADHD) and oppositional defiance disorder (ODD).

Initially it appeared to be working but its effects wore off after just a few hours. Grace began to get sleepy, started confusing her friends, complained of headaches despite her high pain threshold and she lost weight dramatically.

“It just fell off her,” Tracy said.

“At that stage she was going to be put into a mental health unit. Thank god she wasn’t.”

Instead, a mental health worker at CAMHS insisted Grace be given an MRI scan at Timaru Hospital.

It was then doctors discovered two brain tumours, one the size of a golf ball, the other even bigger.

Grace was transferred to Christchurch Hospital last Tuesday and was diagnosed with genetic disorder Neurofibromatosis type 1 – NF1 for short.

The golf-ball sized tumour was drained by 60 per cent in a five-hour operation the following day. But the bigger tumour, which doctors believed had been growing for close to four years, was inoperable.

“It feels like we’re just living in a bubble,” Roger Hooke said. “Our world has been flipped on its head.”

Grace now faces 12 months of chemotherapy at Christchurch Hospital with her parents by her side as doctors attempt to shrink the tumours.

Roger, a truck driver, and Tracy, a Timaru police station staffer, had been given as much time off work as they needed.

A Give a Little page called ‘Saving Grace’ had been started by close friends to help the Hooke family focus solely on treatment. It had raised close to $4000 in donations on Wednesday afternoon.

Grace’s parents said they had been overwhelmed by the amount of support they had received from the community.

They said they were not mad that CAMHS had treated Grace for a behavioural disorder for close to a year.

South Canterbury District Health Board CEO Nigel Trainor confirmed that no complaint had been made by the Hooke’s and Tracy said they would not be making one.

“There’s no point doing that. Hindsight is a great thing but we can’t turn back the clock. We have enough to focus on without being bitter as well.”

Grace went back to school on Wednesday for the first time in three weeks.

“My teacher tried to get me up the stairs and it was hard,” Grace said.

Despite everything she was still smiling, still requesting high fives and still poking her tongue out for the camera.

“You know me mum, I can’t help it,” she said.

Tracy said they were still learning about NF1 and just how rare Grace’s condition was. The tumours were certainly at the extreme end of the condition’s scale because of how long they had gone undetected.

“On so many occasions she should have had a brain scan but she didn’t,” Tracy said.

“I guess what I’d say is that if your gut tells you something wrong, trust it.”

Source: stuff.co.nz

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Breaching The Blood Brain Barrier To Treat Autoimmune Diseases

Efficient delivery of a protein that regulates lymphocyte activation could be one way to treat central nervous system (CNS) diseases such as multiple sclerosis.AsianScientist (Sep. 22, 2015) – Researchers have discovered a cell permeable peptide that can efficiently deliver a conjugated protein through the tightly organized blood brain barrier (BBB). Publishing their findings in Nature Communications, the researchers also showed that the peptide was effective in treating experimental mouse models for central nervous system (CNS) inflammatory disease. Multiple sclerosis (MS) is a demyelinating disease which affects the brain and spinal cord of the CNS. The causes of MS are currently being teased apart, and though no cure currently exists on the market, there are many drugs available to improve the quality of life of patients. “Drugs on the market such as beta-interferons and dimethyl fumarate (DMF), are used to suppress lymphocyte activation, migration and reduction of neuronal cell death,” said Associate Professor Choi Je-Min, a corresponding author of the study from the Hanyang University Department of Life Science. However, a major barrier that prevents effective treatment of such diseases is the efficiency of drug delivery across the BBB. “The BBB is a barrier system that selectively allows the passage of water, some gases and the transport of glucose and amino acids. As such, the BBB represents a huge hurdle to drug delivery into the brain for the treatment of CNS diseases,” Choi told Asian Scientist Magazine. “Therefore, immune modulatory therapeutic proteins or small molecules that might otherwise be suitable for treating MS are limited by their inability to cross the BBB.” In the present study, Choi and his colleagues identified a peptide that would be able to conjugate, penetrate and deliver proteins efficiently into cells. Called dNP2, the peptide was more efficient than other proteins tested at delivering its cargo into primary cells in vitro, a step that normally limits the clinical application of such delivery peptides. The researchers also conjugated dNP2 to fluorescent proteins to allow for peptide tracing after intravenous injections into mice. They observed that dNP2 was efficiently delivered intracellularly to both brain and spinal cord tissue. “This showed that the dNP2-protein complex had successfully crossed the BBB,” said Choi. “If the carrier peptide and the cargo protein complex could be successfully delivered into the brain, we could deliver therapeutic cargo molecules into the brain, which would have huge potential for therapeutic use in human CNS diseases.” Following the identification of a delivery peptide, Choi suggested the conjugation of dNP2 to the CTLA-4 protein, which has been shown to negatively regulate T cell activation, as a novel therapeutic treatment model. “CTLA-4 polymorphisms or mutations are associated with MS and in our study we used the cytoplasmic domain of CTLA-4 (ctCTLA-4) as a therapeutic protein, which has never previously been used for treating MS,” Choi said, adding, “We are the only team to have developed the ctCTLA-4 protein as a therapeutic drug for autoimmune diseases such as MS.” Using this dNP2-ctCTLA-4 conjugate on an experimental autoimmune encephalomyelitis mouse model, a common animal model widely used to represent MS, pathological symptoms such as the infiltration of activated T cells and demyelination were reduced. Considering other CNS diseases that encounters the same BBB hurdle such as Alzheimer’s and Parkinson’s disease, the use of dNP2 as a potential therapeutic agent may be highly effective. “We are currently performing preclinical testing of the dNP2-ctCTLA4 complex in MS in the hope of developing it as a successful therapeutic agent in human neurodegenerative disease.” Choi remarked.

Source: asianscientist

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4 health issues that mess with your memory

Alzheimer’s isn’t the only condition that harms your memory. These four problems can also leave you feeling foggy.

Depression People battling the blues have lower levels of serotonin and norepinephrine—two neurotransmitters that help boost attention and alertness, explains Majid Fotuhi, MD, chair of the Memosyn Neurology Institute and author of Boost Your Brain ($20, amazon.com). The disease is also linked to a smaller hippocampus, according to a 2004 Danish review.

Other symptoms: Fatigue, irritability, trouble sleeping, feeling hopeless, under- or overeating (lasting more than two weeks).

Rx: Your MD will refer you to a psychologist or psychiatrist for counseling and possibly meds.

Hypothyroidism Your thyroid hormones control your metabolism, and if they’re low, it may take longer for nutrients to reach your brain.

Other symptoms: Weight gain, fatigue, dry skin, hair loss, feeling cold.

Rx: Your doc may prescribe synthetic thyroid hormone.

Sleep apnea “When women in their 40s come to my office complaining of memory issues, one of the most common causes is sleep apnea,” said Dr. James Leverenz, Cleveland director of the Lou Ruvo Center for Brain Health at the Cleveland Clinic. The condition causes a closing or narrowing of the airway passages, which can lower oxygen levels in the brain.

Other symptoms: Snoring, gasping, waking up exhausted, morning headaches, daytime sleepiness.

Rx: Remedies include losing weight, avoiding alcohol and possibly using a CPAP machine to keep your airway open with a stream of air.

Celiac disease Researchers aren’t sure how this autoimmune disorder might affect memory, but one theory is that, left untreated, the disease may cause systemic inflammation that can have a negative effect on the brain.

Other symptoms: Fatigue, joint pain, migraines, possibly an itchy skin rash, diarrhea (in about a third of adult cases).

Rx: A small 2014 Australian study found that when celiac patients followed a gluten-free diet, brain-fog symptoms improved within a year.

Source: Fox News

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Could an arthritis drug also help treat Alzheimer's disease?

“Arthritis drug could soon reverse Alzheimer’s symptoms after successful tests on mice,” The Independent reports. The drug – salsalate – may help regulate levels of the abnormal tau protein associated with Alzheimer’s disease, which could improve memory skills.

Salsalate, which belongs to the non-steroidal anti-inflammatory drug (NSAIDs) class of medicines, has been used for many years. And as The Daily Telegraph points out, it was even mentioned by the 5th century BC physician Hippocrates.

This study was conducted in mice with clumps of tau in their brains. Salsalate was given to the mice and was found to block the process that can lead to a further protein build up. Treated mice also performed better in tests designed to assess memory skills.

While these findings show promise, the studies were conducted in mice and were only conducted for a couple of months.

Further human studies will be required to determine how effective the drug is and over what timescale. But because this drug has already been approved for use in humans, these tests may come sooner rather than later.

To reduce your risk of Alzheimer’s disease, a healthy and active lifestyle is recommended. This includes stopping smoking, reducing your alcohol consumption, having a good diet and taking regular exercise.

Where did the story come from?

The study was carried out by researchers from several Gladstone Institutes in San Francisco, the University of California, Stanford University School of Medicine, and the Buck Institute for Research on Aging.

Funding was provided by Tau Consortium and the US National Institutes of Health.

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

This story has been reported in a number of media sources, but it is misleading to say the drug could “soon reverse Alzheimer’s,” as The Independent put it. These findings were in mice, and trials also need to be conducted in humans.

The Daily Telegraph correctly informed readers that, “While there is potential that drugs used to treat other diseases could be of benefit in dementia, nobody should be taking such drugs until clinical trials have shown them to be safe and effective for the treatment of dementia.”

Salsalate can be dangerous for certain groups of people, such as those recovering from heart surgery. You should never take salsalate unless it’s been prescribed for you by a qualified doctor.

What kind of research was this?

This animal study in mice investigated the changes occurring in the brain in a mice model of the early stages of Alzheimer’s disease.

This condition is characterised by the accumulation of tau proteins and a reduction in brain volume, especially in an area called the hippocampus, which is important for forming memory.

Further investigation was carried out to assess the effect of the prescription drug, salsalate, on the accumulation of tau proteins and brain volume.

While this is a good method to investigate effects, any findings would have to be confirmed in humans.

What did the research involve?

Researchers used human brain samples to investigate how the tau protein builds up in the brain in Alzheimer’s disease.

They identified how greater levels of tau acetylation – a chemical process that alters the tau protein, causing it to build up and induce cognitive defects – was associated with progression of disease.

The study then involved laboratory mice with dementia to firstly confirm a similar mechanism of tau acetylation and disease, and then test the effect of salsalate on disease progression.

Mice with dementia and normal mice were assigned to receive salsalate or a placebo daily. Female mice aged eight to nine months were treated for a total of 60 days, and male mice aged seven to eight months were treated for 84 days. Brain volume was assessed at the end of the trial.

Behavioural tests for spatial learning and memory retention were conducted on the 35th day for female mice and about the 60th day for the male mice. Investigators who performed the dosing and behavioural tests were blinded to the type of mice or treatment received to reduce the risk of bias.

What were the basic results?

The study identified a chemical change called tau acetylation as an early change in Alzheimer’s disease brains in mice. The altered tau protein is slow to break down, causing an accumulation and leading to cognitive decline.

Researchers found salsalate prevented the chemical change occurring, allowing the tau protein to break down as normal and reducing its build up.

At eight months, the brain volume in the hippocampus was the same in both groups of female mice. After treatment at 10 months of age, the volume had reduced in mice with dementia that had been given a placebo.

In mice with dementia given salsalate, there was no reduction in brain volume compared with normal mice, showing it had halted this part of the disease process. Similar results were found for the male mice.

How did the researchers interpret the results?

The researchers concluded salsalate lowers levels of tau protein with protective effects.

Targeting tau acetylation could be a new therapeutic strategy against neurodegenerative disease, they say.

Conclusion

Salsalate was found to inhibit the tau acetylation process and prevent an accumulation of the tau protein in the brains of mice. It was also found to improve memory retention and prevent the loss of hippocampal brain volume.

However, we do not know whether salsalate would replicate the effects observed in mice when used in humans. But these findings do provide a route for further research in a drug already prescribed to people with arthritis.

Although we are aware of the potential side effects at doses suitable to help arthritis, we don’t know what dose may be required to be effective against dementia. This could alter the side effect profile if the dosage needs to be higher.

It is unclear whether this drug is actually prescribed in the UK, as it is unlicensed for use in this country. Salsalate is also currently being used in a clinical trial for another brain disease.

Other ways to reduce your risk of Alzheimer’s disease include stopping smoking, lowering your alcohol intake, eating a good diet and taking regular exercise.

Source: nhs

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Low Levels of Vitamin D Might Hurt Your Brain

Health experts have long known that vitamin D isimportant for healthy bones and teeth. It may also helpto protect the body against diseases such as diabetesand cancer. And now, researchers say vitamin D mighthelp fight brain diseases called dementias.

Dementias are brain diseases that damage thinking and memory processes,what scientists call “cognitive abilities.” Dementias are difficult to treat.Taking care of someone who has dementia is extremely demanding. And thedisease is very frightening to sufferers.

Chris Roberts suffers from dementia. He says the worst part of living with thisdisease was getting lost while driving.

“The worst thing that I found was getting lost in the car, not just forgettingwhere I was going - I wouldn‘t know where I was.”

More than 47 million people around the world suffer from dementia. The WorldHealth Organization reports that 60 percent of them live in low- and middle-income countries.

Now a new study in the United States shows a possible link betweendementia and low levels of vitamin D.

From where do we get vitamin D?

We get vitamin D from some foods like nuts, lentils and fatty fish like salmonand mackerel.

We also get vitamin D from the sun. But that is notdependable. In some parts of the world, there is notenough sunlight to provide enough vitamin D.

Also, sunblock substances prevent the vitamin fromentering the body. To add to the problem, the skin’sability to process vitamin D weakens as a person ages. As a result, low levels of vitamin D are common amongolder people.

Researchers at Rutgers University in New Jersey areexploring the relationship between vitamin D and dementia. The team recentlymeasured vitamin D levels and cognitive ability in older people.

Nutritional sciences professor Joshua Miller led the team. He said cognitiveabilities differed among the study subjects. He said tests showed that about60 percent of the group was low in vitamin D.

“Some of the subjects had outright dementia, some had mild cognitive impairment and some had what we would call normal cognitive functioning.”

Those subjects who had low vitamin D levels showed more short-termmemory loss. They were also less able to organize thoughts, order tasks byimportance and make decisions.

“Those who had dementia also had lower vitamin D status than those whohad mild cognitive impairment or who had normal cognitive functioning.”

The findings suggest that vitamin D might play a part in slowing dementia. But,more studies are needed to see if vitamin D supplements could help.

Source: learningenglish

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Alberta girl denied marijuana for epilepsy gets help in St. Catharines

An Alberta mother whose daughter has severe epilepsy has travelled to St. Catharines, Ont. for a medical marijuana prescription after the girl’s doctor said he was no longer allowed to provide permission to purchase the product.

In 2013, Sandra Wilkinson had started extracting cannabis oil from dried marijuana — purchased from a licensed grower with a prescription from a neurologist at Alberta Children’s Hospital — to prevent life-threatening seizures in her eight-year-old daughter Mia.

But in July, the physician declined to renew the prescription because of a hospital policy based on the position of Alberta Health Services, the provincial health authority, which does not support the use of medical marijuana for pediatric patients with epilepsy.

Wilkinson said the cannabis oil is the only therapy that has worked to stop Mia’s seizures, caused by a rare type of epilepsy called Ohtahara syndrome.

Despite taking 30 to 40 anti-convulsive pills daily, Mia would suffer up to 100 seizures a day, said her mother. But since starting daily doses of oral cannabis oil 19 months ago, she has not had a single seizure.

On Monday, Mia was seen by a doctor at the Canadian Cannabis Clinic in St. Catharines, and left with a prescription for dried marijuana, which her mother can fill from a federally licensed producer after returning to their Airdrie, Alta., home.

“It’s a big relief. I don’t have to worry about when I run out of her meds,” said her mother, who had been worried about her dwindling supply of medical-grade marijuana purchased with the initial prescription.

Wilkinson said she turned to cannabis because nothing else was helping her child, whose seizures could be so severe she would stop breathing and have to be resuscitated and rushed to hospital.

‘She would have died’

“I really took a big leap of faith with that,” she said of the cannabis oil, adding that within 24 hours of the first dose, Mia’s seizures had completely stopped.

Without the treatment, “we would have waited for the next big seizure and she would have died. There’s not a really nice way to say that.

“Now, we can all breathe.”

For Mia, tetrahydrocannabinol, or THC, appears to be the ingredient in marijuana that controls her seizures, while others with different forms of epilepsy benefit from another component of the plant called cannabidiol, or CBD.

Pharmacologist-toxicologist McIntyre Burnham, co-director of the Epilepsy Research Program of the Ontario Brain Institute in Toronto, said about 30 per cent of people with seizures don’t respond to any anti-convulsive medications.

His program plans to seek Health Canada approval for a clinical trial in adults of a cannabidiol in capsule form being developed by Canadian medical marijuana producer Tilray, which he hopes will start in about a year.

While THC does stop seizures in some people, it’s also the active ingredient in marijuana that “makes you high,” said Burnham, whereas CBD does not.

Researchers agree clinical trials are needed to determine if the various strains and extracts of marijuana can benefit patients with a variety of conditions, and cannabidiol appears “quite promising” for epilepsy, he said.

But “people are thinking it’s a wonder drug. I think it’s too early to say that … It’s not going to be for everyone. It will help some people and not help others.”

Kunvar Mudhar does believe CBD is a wonder drug.

‘A miracle’

A year ago, she started giving cannabis oil high in CBD to her son Zen, who has intractable epilepsy related to cerebral palsy that is resistant to all anti-convulsive medications.

As a baby, he had been put on a special diet, which reduced the number and severity of his seizures — but he was still experiencing about 150 a day.

“The first night I gave him the first dose, we started off very low,” said Mudhar of Mississauga, Ont., who makes cannabis oil from dried marijuana purchased through a doctor’s prescription.

Within a day, the number of Zen’s seizures dropped to about 30, and with a slight increase in the dose, they disappeared for months.

Mudhar had been treating Zen, now 7, with an oil high in CBD and low in THC, but she also had on hand an oil extract she’d prepared with a two-to-one ratio of CBD to THC.

One night in February, her son suffered a grand mal seizure, despite the daily cannabis therapy.

“His body was jerking. He started to turn grey-blue,” she said. “At that point, I had nothing else to give him. I had already called the paramedics and was waiting for them to come.

“The last thing I did was grab that (higher THC-dose) oil and rub it on his gums — and the seizure stopped.”

Mudhar said she would have been happy if the cannabis oil had just reduced his seizures by a significant amount.

“But this is amazing. To me, this is more than a miracle that Zen has seizure-free days.”

Source: CBC Hamilton

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Clinic Claims It Can Cure Cancer and Autism with Tobacco Smoke

Most doctors claim tobacco smoke causes serious diseases, but at the Griya Balur clinic, in Indonesia, it’s used as a cure for cancer, autism or emphysema.

In most western countries, a clinic that uses tobacco as a remedy would have been closed down immediately, but in the city of Jakarta, it’s one of the busiest treatment centers. People suffering from serious illnesses, some ironically caused by years of smoking, come to Gryia Balur searching for miraculous cures associated with tobacco smoke. Its founder, Dr Gretha Zahar told AFP that she has treated over 60,000 people from all over the world, in the last ten years.

The treatment for cancer or emphysema sufferers includes blowing smoke from “divine cigarettes” infused with “nanotechnology”, through a tube, to remove cancer-causing “free radicals”. Smoke is blown into the mouth, nose and ears of the patients.  Zahar claims that smoking actually manipulates the mercury found in tobacco cigarettes, curing deadly diseases and even slowing down the aging process. On her website, she says her theories don’t need to be published in medical journals or subjected to clinical tests, and that she doesn’t have the financial resources to “fight Western medical scientists”.

With tobacco cigarettes becoming more and more popular in Indonesia, Griya Balur clinic is in no danger of being shut down, as the government collects around $7 billion a year in industry taxes. Old traditions relating to tobacco, and aggressive advertisements from cigarette companies hoping to gain a new foothold in the area, after losing ground in the western world, are causing an increasing number of young Indonesians to take up smoking

According to the World Health Organisation, 400,000 Indonesians die from cigarette smoking  every year, while another 25,000 die from passive smoking, but that hasn’t stopped some tobacco farmers and legislators from challenging a law that recognizes the plant as addictive and hazardous to health. They recently went to court invoking Dr. Zahar’s theories and claiming tobacco is in fact a cheap alternative to more expensive drugs, and that it eliminates anxiety, calms the nerves and increases concentration. A pharmacology professor even told the judges he has never heard of anyone dying from smoking…

Source: Jakarta Globe

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Mind Control Programs Exposed – Your Thoughts Are Not Your Own

Research into the structure and function of the human brain continues to accelerate. Collaborations, such as the Human Brain Project in Europe and the BRAIN initiative in the United States, are exploring making great advances in understanding the brain’s circuitry and computing principles.

The supposed goals of these research initiatives are to understand the cause of and to improve treatment of brain disorders, to create neuromatic and neurorobotic technologies that advance developments in Artificial Intelligence and supercomputers, and also to uncover the patterns of neural activity that produce human cognition, decision making and actions. In 2014, over $300 million in public and private funding was made in support of the US BRAIN initiative, and EUR 8.3 million was invested in the European Union’s Human Brain Project.

Simultaneously, technologies are being developed to create a new brain-computer interface, which will be able to manipulate the brain using “neural dust,” light beamed from outside the skull, and by implanting memories by altering neuron DNA.

The human mind is an electrical device. If they reverse engineer the brain to figure out how to invade and program the electrical mind, it can be taken over and anyone can theoretically be controlled remotely, and the affected persons would have little to no clue what was going on.

In the interviews below, Neil Sanders, author of Your Thoughts are Not Your Own, and Steven Jacobson, author of Mind Control in the U.S., expose evidence of officially sanctioned mind control programs and the effects of media programming on human behavior.

As innovations that understand and alter brain function continue to mature, can we trust their creators to use them to benefit humanity, versus using them to further manipulate the masses and influence specific individuals?

Source: Waking Times

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Taking a daily vitamin D supplement 'can ward off dementia': Over 60s with deficiency found to experience quicker mental decline

Older people should boost their intake of Vitamin D with supplements to ward off dementia, a new study suggests.

Researchers have found people over the age of 60 with low levels of the essential vitamin experienced mental decline up to three times faster than those with adequate readings.

Vitamin D – known for its importance for bone health – is obtained primarily through sun exposure as well as egg yolks, cheese and fish oil.

The new study, published in the journal Neurology, discovered that it also has a major impact on how the body, including the brain, functions.

Joshua Miller, professor of nutritional sciences at the Rutgers School of Environmental and Biological Sciences in the US, said: ‘There were some people in the study who had low vitamin D who didn’t decline at all and some people with adequate vitamin D who declined quickly.

‘But on average, people with low vitamin D declined two to three times as fast as those with adequate vitamin D.’

The study, involving 382, people took place over an eight-year period between 2002 and 2010.

Source:  Mail Online

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Alzheimer's Disease Transferred Through Human Growth Hormone

Researchers at the University College of London think they’ve found a link between human growth hormone and the development of the neurodegenerative disease. By studying the brain tissue of eight recipients who died of Creutzfeldt-Jakob disease (CJD) after being injected with the hormone, the scientists discovered that the recipients also had signs of early onset of Alzheimer’s. In short, if the disease can be passed through hormones, then the disease might not be entirely a genetic disorder.

Of course, other scientists are doubtful — mainly because it is extremely difficult to determine the paths of disease transmission. Nevertheless, there is evidence that mice can contract Alzheimer’s by being injected with proteins from Alzheimer’s patients.

In short, if the disease can be passed through hormones, then the disease might not be entirely a genetic disorder.

Understanding how a disease develops is obviously key to treating those who suffer from it. The most popular treatments are medications that help increase the brain’s levels of acetylcholine, a chemical that helps neurons transmit information to one another. However, a recent study found that resveratrol — the antioxidant found in red wine and chocolate — can change the amyloid-beta ratios in the brain (amyloid-beta is a neuro-protein), which in turn helped to slow the progression of the disease.

If Alzheimer’s is indeed contagious, that could change how doctors treat it and other so-called genetic diseases as well. Already,epigenetics — or cellular genetics that considers the impact that environmental factors have on genes — has determined that diet can change the make-up a person’s DNA that can then be passed on to his or her offspring.

In one study, Swedish scientists examined the genes of people who had died of cardiovascular disease and diabetes and found that availability of food to a father or grandfather before puberty was directly correlative to the development of these diseases in their children and grandchildren. Perhaps then with Alzheimer’s, the “contagious” aspect could be related to how genes change or develop when exposed to influencing hormones and proteins.

Source: bigthink.com

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Brain-Machine Interface Learns to Control Robot Arm Based on User’s Error Brain Signals

Brain-machine interfaces (BMIs) restore or replace motor or sensory function in individuals who are disabled by neuromuscular disorders, stroke, or spinal cord injury. Electrical signals, acquired through either invasive or non-invasive neural interfaces, are decoded to subsequently control external devices. However, patients must spend a significant amount of time training their brain to successfully control such neuroprosthetic devices.

Jose Millán’s group at École Polytechnique Fédérale de Lausanne in Switzerland have published in Nature Scientific Reports a BMI paradigm that enables neuroprosthetic devices to learn on the fly, thus decreasing patient training time. The technology is based on the error-related potential (ErrP) measured non-invasively using electroencephalographic (EEG) electrode arrays. The ErrP is elicited when an error is made, or when the action does not match the user’s expectation. The user’s error signal is integrated into the neuroprosthetic controller, enabling the neuroprosthetic device to learn incorrect movements and modify its behavior.

Twelve subjects trained the ErrP decoder to detect their individual ErrP signals by observing 350 robot movements where 20% of the movements were incorrect (robot arm moved away from the target). The average time to train the ErrP decoder was merely 25 minutes. Then, in the most complicated of three experiments, the subject controlled a real robot arm to move in 2D space (right, left, up, and down) to reach a target location. At first, the robot moved randomly, but subsequently adapted its movements based on the detection of the subject’s ErrP signals.

Here’s a video of a volunteer controlling a robotic arm powered by the new error correcting approach:

Source: Medgadget

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Canadian advance in solving brain disease

Brain disease is mysterious, deadly,  and in the interim extremely troubling to the victim and to family and friends.

It’s also troubling to medical researchers who are constantly looking for ways to combat diseases for which, as of yet, little can be done.

One of those diseases is prion disease, known as Creutzfeldt-Jakob Disease (CJD) in humans, but also as the more common cattle disease bovine spongiform encephalopathy, (BSE), the so-called “mad-cow disease” or scrapie in sheep.

There is no cure for these diseases.

However, research in Canada has made a step in that direction. Valerie Sim  (MD) is an assistant professor in the University of Alberta’s Faculty of Medicine & Dentistry

Dr. Sim supervised the research team and her research associate Leonardo Cortez (PhD) was the lead author of the paper published in  the Journal of Virology under the title, Bile Acids Reduce Prion Conversion, Reduce Neuronal Loss, and Prolong Male Survival in Models of Prion Disease

Whether in animals or humans, “prion” disease (BSE, CJD and others) causes physical destruction within the brain such that it starts to look like swiss cheese. The effects are the same in animals or humans.  As the disease rapidly progresses, patients with CJD may experience any or all of the following symptoms:

:  visual deterioration and eventual blindness, dementia, involuntary muscle contractions, loss of balance, memory loss,  incoordination, slowed movement, personality change, and within just a few months, death.

One of the reasons that BSE/ mad-cow disease causes such concern is that has been shown that consuming meat from infected cattle can transmit the disease to humans. It should be pointed out that the most common form of the disease however, is not from eating meat CJD and it should be pointed out that it is very rare at one or two persons per million per year.

Prion proteins are found in the brain, and are a normal part of the body and brain function. They can be broken down, but if a prion protein becomes misshaped for whatever reason as it folds, it cannot be broken down.

The disease really starts as the misshapen prion protein can then begin to change the form of other prion proteins around it causing them to become misshapen as well.  This results in a chain reaction as they begin changing other prion proteins around them which quickly kills brain cells and soon leaves actual holes in the brain.

Although not exactly the same, Alzheimers is a similar type of protein disease, as is Parkinson’s.

The research team examined the effect of two compounds the body produces. These are bile acids made by the liver called UDCA (ursodeoxycholic acid) and TUDCA (tauroursodeoxycholic acid).

These have been used in Chinese traditional medicine, and other research had shown they exhibit some slowing effects on the spread of similar protein diseases in research models. These acids normally help to break down fats and lipids that are eaten but in testing with prion disease, it appears they bind the misfolded prion proteins to prevent them spreading to other prion proteins, and to also block the pathways into brain cells leading to cell death.

Dr. Sim notes that the bile compounds would have to be administered very early in the disease, and that usually by the time patients come to medical attention, it’s already too late.

She says it might prove useful in those rare cases where there is an inherited genetic factor.

“Some of those people know they are carriers of the disease and currently we have nothing we can give them that works,” says Sim. “This is not a cure, but may have some benefit if given early. And for these patients, any benefit is better than nothing.”

Dr. Sim says clinical applications however are still years away, and research continues to test a combination of UDCA and TUDCA with other anti-prion compounds, and to determine for example if this would have long-term benefits for patients, or merely prolong life at the end stage of the disease.

Dr. Sim notes that such advances in finding cures for difficult diseases are often built on results from other studies unrelated to the disease research and as such highlights the importance of “pure science research”.

She also says for now the best way to protect oneself from the most common forms of brain disease is by getting exercise, sleep, and by not smoking.

Research funding was provided by Alberta Innovates – Bio Solutions, Alberta Innovates – Health Solutions, and the University Hospital Foundation.

Source: rcinet.ca

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Epilepsy: sorting the myths from the facts of a common disorder

One of AFL’s biggest stars, Lance Franklin, was briefly hospitalised for a mild epileptic seizure last week. He was also ruled out of Saturday’s qualifying final, as he is reportedly suffering from an “ongoing mental health condition”.

Although they may coexist, epilepsy is a neurological disorder that doesn’t fall under the umbrella of mental or mood disorders. But the likelihood of mood disorders, such as depression and anxiety, increases with chronic brain illnesses. And there may be a slight further increase if you have epilepsy.

People with epilepsy need treatment, but also understanding they are normal, capable people. Unless someone has a noticeable seizure in a public place, you won’t know they have epilepsy. There’s no abnormality, as such, springing from the illness. Nor is there a limit to what someone with the condition can accomplish.

Understanding epilepsy

Globally, epilepsy is one of the most common neurological diseases, particularly among children. Epilepsy is not a single disorder; it has many causes that share the hallmark of a seizure, when brain function is disrupted, often dramatically. When seizures remain isolated in just one part of the brain, they can be very small and can even pass by unnoticed.

But when seizures involve large parts of the brain, the consequent event is what people typically associate with an “epileptic fit”. The person’s muscles stiffen, they lose consciousness and fall to the floor, and their body starts jerking rhythmically. These types of seizures are called “tonic-clonic” seizures - because the body is first stiff all over (tonic) and then has rhythmic jerking (clonic).

Seizures can be frightening for those who have never witnessed one before. Historically, the loss of control of the body and brain that came with having an epileptic seizure was often misunderstood. The biblical story of Jesus performing an exorcism on a young boy having a seizure, for instance, led some to believe they were a result of demonic possession. Only in modern times has epilepsy been truly recognised as a disease of the brain.

There are still misunderstandings, though. It’s wrong to think, for instance, something should be put into the mouth when someone is in the middle of a seizure; it’s not true that the tongue can be “swallowed”. First aid is applied to prevent injury while the person is stiff and jerking, but when they go limp at the end of the seizure, they should be put on their side to prevent the floppy tongue obstructing breathing. After a seizure, it may take some time for behaviour to return to normal and sleepiness is common.

Epilepsy is a diverse condition that can have many, different causes from shutterstock.com

Treatment options

Saying someone has epilepsy is a little like saying that they’re ill. Its cause is diverse and can be anything from a brain tumour to an inherited genetic condition, the consequence of injury, or any other disorder that affects the brain. In some cases, epilepsy is associated with other brain problems and intellectual disability. But mostly, people with epilepsy are normal between seizures and can participate in normal activities. If seizures are not controlled, then operating dangerous machines, like cars, or swimming unsupervised must be avoided.

Most epilepsy is well controlled with medications. Options for treatment have expanded with new drugs available, more precise diagnosis based on sophisticated imaging, and better understanding of the mechanism of epilepsy in each individual patient. In some cases, very precise detection of brain lesions can allow for a surgical cure of epilepsy. Even devices used as brain implants have been developed that can control severe epilepsy.

It’s common for some mood disorders also to be present in people with epilepsy. Naturally, the fear of having an unexpected seizure can directly lead to an anxiety disorder, while the stress of coping with chronic illness can contribute to depression. In some types of epilepsy, the brain networks that give rise to the illness may also make people more vulnerable to these co-morbidities. It is important that both problems are properly assessed and diagnosed.

For someone like Lance Franklin, simply “carrying on” if there is a mental or neurological problem would be as bad as “playing on” with a muscle problem that was not recognised and treated. Like the physical side of sport, where an optimised musculoskeletal system is important, so it’s important to recognise that the brain needs just as much care, effort and medical attention.

Source: theconversation.com

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