Parkinson’s disease: Stages, symptoms, causes, and natural treatment

November 12, 2016  By: Bel Marra Health | Brain Function 

For years, little was known about Parkinson’s disease. Without a cause, a cure could not be found. But after extensive research, we’re closer to a potential cure as scientists have now discovered a cause for Parkinson’s disease.

Parkinson’s disease mainly affects movement as it is a progressive neurological illness. Which means, over time Parkinson’s disease worsens. Sufferers of Parkinson’s disease will experience tremors in their limbs and even stiffness and lack of movement, which will only get worse as time goes by.

This occurs because of damage in the nerve cells within the brain. The damaged neurons – substantia nigra – contain dopamine, a chemical that controls movement. Damaged and lower amounts of dopamine lead to changes in bodily movement, even limiting the ability to move.

Stages of Parkinson’s disease

Parkinson’s disease comes in five stages, and it’s not uncommon for the patients to skip over stages, which means symptoms may worsen more rapidly.

Stage 1: Symptoms are mild and the patient may experience slight tremors in hands and arms on one side. Posture, balance, and facial expressions are affected and are noticeable.

Stage 2: Symptoms have now progressed to affect both sides of the body. Walking and balance become impaired, and difficulty arises when completing tasks.

Stage 3: Symptoms are quite severe and person may be unable to walk in a straight line or keep their balance. Physical movements also become much slower.

Stage 4: Walking becomes limited, movements are very slow, and daily tasks are hard to complete – patient may require an assistant or even a live-in caregiver.

Stage 5: Nursing care is highly required as person has lost all major abilities to perform tasks, walk, or care for themselves.

Symptoms of Parkinson’s disease

Parkinson’s disease symptoms include:

• Tremors in the arms, hands, legs, and jaw. May start off on one side of the body, then progress to both.
• Bradykinesia, which refers to slow movements
• Rigidity – limbs and torso become stiff
• Impaired balance and coordination
• Changes in speech
• Impaired ability to write

As you can see, all major bodily movements become affected by Parkinson’s disease. As symptoms and stages of Parkinson’s disease progress, more abilities become impaired.

Study: Real cause of Parkinson’s disease revealed

Now that we have a better understanding of what Parkinson’s disease is and how it affects the body, let’s look at the latest study that reveals a possible cause of this illness.

The new findings come for the University of Cambridge. Researchers have successfully identified the role of alpha-synuclein (a protein in the brain) in the cause of Parkinson’s disease.

Usually, this protein helps chemical signaling in the brain to work properly. If this protein exceeds its threshold, it begins to clump together. Clumping of alpha-synuclein results in toxicity, which then brings on the onset of Parkinson’s disease.

To better understand this concept, think of cholesterol. When the levels of LDL, or bad cholesterol, increase, our arteries begin to clog, so oxygen-rich blood cannot travel through. This can lead to serious health problems over time.

One’s risk of developing Parkinson’s disease is then determined by this balance of proteins – alpha-synuclein and synaptic vesicles. Synaptic vesicles carry neurotransmitters to the nerve cells. Cells reproduce vesicles, so this exchange can continue to occur. Alpha-synuclein is responsible for releasing these neurotransmitters. When alpha-synuclein doesn’t bind and fold properly, that is when they can become toxic and turn into Lewy bodies. Lewy bodies are also found in Alzheimer’s disease.

Researchers are hopeful that their new findings can offer a better understanding of Parkinson’s disease and, in turn, help find a cure for the illness.

Parkinson’s disease treatment with natural remedies

Although the new research seems promising, it will still be quite some time until a cure for Parkinson’s disease will come about. In the meantime, here are some suggestions to help manage this condition.

Eat healthy: Healthy eating is a trademark treatment for all illnesses. What we eat can either worsen or slightly improve a condition. This is no different in those with Parkinson’s disease. A balanced meal is essential for Parkinson’s patients as it provides nutrients required for the body as a whole to function properly.

Exercise: Because Parkinson’s disease can cause stiffness in the body, it’s important to try and exercise to maintain muscle, mobility, and balance. Exercising within your limits and with the help of a physical therapist may aid in boosting movement and improving balance.

Avoid injury: It’s important that those with Parkinson’s disease avoid injury at all cost, especially falls. Exercise may help with stability, but avoid walking backwards, do not pivot on your feet, and avoid carrying objects while walking.

Parkinson’s disease can greatly affect one’s life, and we are now one step closer to combating this debilitating illness. Although there isn’t a proven method of preventing Parkinson’s disease, eating well and staying active can make for a strong and healthy body.

http://www.belmarrahealth.com/parkinsons-disease-stages-symptoms-causes-natural-treatment/

PEPTOIDS AS A BIOMARKER FOR PARKINSON'S DISEASE

12th November 2016 

Costly methods of diagnosis such as the SPECT scan or the PET scan are used for the indication of Parkinson's Disease. However, in early Parkinson's Disease a far less costly and relatively non-invasive biomarker would be preferable.

Researchers have identified a peptoid called PD2, which significantly binds higher levels of IgG3 antibody in those people with Parkinson's Disease. The PD2 peptoid was found to be 68% accurate in identifying Parkinson's Disease, which is less accurate than existing methods. 

However, PD2 was 84% accurate in identifying new cases of Parkinson's Disease. It is new cases of Parkinson's Disease that existing methods are not so accurate with. PD2 levels are also positively correlated with the United Parkinson's Disease Rating Scale score, which is the primary symptom questionnaire for Parkinson's Disease. So the researchers concluded that PD2 may be useful for the diagnosis of early Parkinson's Disease.

Reference : NPJ Parkinsons Disease [2016] 16012 Epub Jun 23 (U.Yazdani, S.Zaman, L.S.Hynan, L.S.Brown, R.B.Dewey, D.Karp, D.C.German)

Complete abstract : http://www.ncbi.nlm.nih.gov/pubmed/27812535 

http://www.viartis.net/parkinsons.disease/news/161112.pdf mail@viartis.net

Pain is Not Just a Matter of Nerves

NEUROSCIENCE NEWSNOVEMBER 11, 2016

Summary: Researchers reveal the role glial cells play in the sensation of pain.

Source: Medical University of Vienna.

Over-activation of glial cells in the spinal cord can, for example, be caused by strong pain stimuli from a wound or surgical intervention, or even by opiates. Neurosciencenews image is adapted from the Medical University of Vienna press release.

The sensation of pain occurs when neural pathways conduct excitation generated by tissue damage to the spinal cord, where the nociceptive information is extensively pre-processed. From there, the information is transmitted to the human brain, where the sensation of “pain” is finally created. This is the general belief. However, researchers from the Division of Neurophysiology at MedUni Vienna’s Center for Brain Research have now discovered that pain is not just a matter of nerves but that non-neuronal cells, the glial cells, are also involved in clinically relevant pain models and their activation is sufficient to amplify pain. The study has now been published in the leading journal “Science”.

Glial cells are the commonest type of cells in the human brain and spinal cord. They surround neurons but are distinct from them and play an important supporting role – for example, in material transport and metabolism or the fluid balance in the brain and spinal cord.

Novel explanation for puzzling pain phenomena

At the same time, however, when they are activated – by pain processes, for example ­– glial cells are themselves able to release messenger substances, such as inflammatory cytokines. Glial cells therefore have two modes: a protective and a pro-inflammatory mode. “The activation of glial cells results in a pain-amplifying effect, as well as spreading the pain to previously unaffected parts of the body. For the very first time, our study provides a biological explanation for this and for other hitherto unexplained pain phenomena in medicine,” says Jürgen Sandkühler, Head of the Division of Neurophysiology at MedUni Vienna’s Center for Brain Research.

Over-activation of glial cells in the spinal cord can, for example, be caused by strong pain stimuli from a wound or surgical intervention, or even by opiates. Sandkühler: “This could also explain why opiates are initially very good at relieving pain but then often cease to be effective. Another example is the phenomenon of “withdrawal” in drug addicts, where activated glial cells cause severe pain throughout the body.”

A healthy lifestyle can beneficially impact the glial cell system

According to Sandkühler, neuroinflammatory diseases of the brain, environmental factors and even the person’s own lifestyle can lead to activation of glial cells. Examples from the current literature are: depression, anxiety disorders and chronic stress, multiple sclerosis or Alzheimer’s and diabetes, as well as lack of exercise and poor diet. Sandkühler: “Glial cells are an important factor in ensuring the equilibrium of a person’s neuroinflammatory system.” The study results give grounds for speculation that improvements in a person’s lifestyle could have a beneficial impact upon this system and ensure that they generally suffer less pain or “minor niggles”, says Sandkühler: “It is therefore in our own hands: thirty minutes of moderate exercise three or four times a week, a healthy diet and avoiding putting on excess weight can make a huge difference.” 

ABOUT THIS PAIN RESEARCH ARTICLE

Source: Medical University of Vienna
Image Source: This NeuroscienceNews.com image is adapted from the Medical University of Vienna press release.

Original Research: Abstract for “Gliogenic LTP Spreads Widely in Nociceptive Pathways” by M.T. Kronschläger, R. Drdla-Schutting, M. Gassner, S.D. Honsek, H.L. Teuchmann, and J. Sandkühler in Science. Published online November 10 2016 doi:10.1002/da.22577

Abstract

Gliogenic LTP Spreads Widely in Nociceptive Pathways

Learning and memory formation involve long-term potentiation of synaptic strength (LTP). A fundamental feature of LTP induction in the brain is the need for coincident pre- and postsynaptic activity. This restricts LTP expression to activated synapses only (homosynaptic LTP) and leads to its input specificity. In the spinal cord, we discovered a fundamentally different form of LTP that is induced by glial cell activation and mediated by diffusible, extracellular messengers, including D-serine and tumor necrosis factor (TNF), and that travel long distances via the cerebrospinal fluid, thereby affecting susceptible synapses at remote sites. The properties of this gliogenic LTP resolve unexplained findings of memory traces in nociceptive pathways and may underlie forms of widespread pain hypersensitivity.

“Gliogenic LTP Spreads Widely in Nociceptive Pathways” by M.T. Kronschläger, R. Drdla-Schutting, M. Gassner, S.D. Honsek, H.L. Teuchmann, and J. Sandkühler in Science. Published online November10 2016 doi:10.1002/da.22577

http://neurosciencenews.com/neurons-pain-amplification-5489/

Electrotherapy: Shock value

27 October 2016

• Michael Eisenstein

Deep brain stimulation is a proven treatment for Parkinson's disease. The only thing left to find out is how it works.

Coloured X-ray showing electrodes being implanted for deep brain stimulation.

Before your doctor starts sticking electrodes into your brain, it would be reasonable to hope that he or she knows precisely what will happen and why. But when it comes to deep brain stimulation (DBS) for Parkinson's disease, the only thing the experts can agree on is that it works.

In DBS, millimetre-thin electrodes are implanted into the brain, aimed at a target smaller than a corn kernel, the location of which has been painstakingly mapped from imaging data. The electrodes deliver a mild stream of electrical jolts to the subthalamic nucleus that can control the debilitating motor symptoms that patients experience.

Over the past few decades, the medical community has embraced this treatment. “The procedure is very safe and effective,” says Andres Lozano, a neurosurgeon at the University of Toronto in Canada. He estimates that around 10,000 people worldwide undergo DBS surgery for Parkinson's every year, with more than 140,000 people receiving implants so far. Yet little is known about how DBS restores normal function to the brain's motor circuitry.

Progress is being made, however, and any advance in the understanding of the disease could yield major dividends in patient-specific care. “We are just blasting the brain with continuous stimulation at the moment, and it's amazing that such a crude intervention helps so much,” says Jill Ostrem, a neurologist at the University of California, San Francisco (UCSF). “Imagine what we could do if we could be more sophisticated and individualistic about this.”

Circuit Breaker

Parkinson's Disease

Perhaps the biggest obstacle is the continuing uncertainty about how Parkinson's causes the brain's circuits to malfunction. Most research into the neurophysiology of the disease has focused on the brain's 'motor circuit', which consists of the basal ganglia, the thalamus and part of the cortex that governs movement. As Parkinson's progresses, neurons in the basal ganglia that produce the neurotransmitter dopamine die, derailing the function of the motor circuit. “Dopamine plays the major role in setting the rules for neural activity,” says Lozano. “In the absence of that influence, the neurons start misbehaving and firing in a pattern that is pathological.”

At first, researchers seeking an explanation for the neurons' misbehaviour favoured what was known as the 'rate model', which was developed in the 1980s. Neurologist Mahlon DeLong at Emory University in Atlanta, Georgia, proposed that parkinsonian symptoms arise from a higher rate of signalling in a region of the basal ganglia known as the subthalamic nucleus. DeLong thought that this increased neuronal firing was inhibiting other areas in the motor circuit, and reported that surgical disruption of the subthalamic nucleus relieved parkinsonian motor symptoms in monkeys¹. In the 1990s, Alim-Louis Benabid and his colleagues, then at the University Hospital of Grenoble in France, used DeLong's findings as a foundation for the development of DBS for Parkinson's. Benabid's team demonstrated that high-frequency electrical stimulation, delivered by electrodes positioned near the subthalamic nucleus, eased motor symptoms such as rigidity².

The electrodes are targeted to the tiny 

subthalamic nuclei (white arrows) for 

deep brain stimulation.

Although the fundamentals of how DBS is given to people with Parkinson's have changed little since then, the rate model has largely fallen by the wayside. Instead, it seems that symptoms arise from a change in the normal firing patterns across the motor circuitry, rather than excessive firing at one point. The concept now is that the circuit is excessively synchronized, says Philip Starr, a neurosurgeon at UCSF. “Individual cells in the motor cortex and the basal ganglia that normally tend to fire independently now fire together,” Starr explains. In particular, Parkinson's researchers have identified high levels of β-band oscillation — brainwave activity occurring at around 15–30 hertz — within the basal ganglia. Such frequencies also occur in the healthy brain but become exaggerated in Parkinson's and seem to be associated with delayed or impaired conscious movement.

Normally, dopamine-producing neurons in the basal ganglia  prevent such synchronized rhythms from
becoming established; in this 'pattern model', the loss of these neurons removes this safeguard. But researchers are still unclear how the disruptive β activity arises. One possibility is that the activity spills over from other connected regions of the brain. Neurologist Helen Bronte-Stewart, at Stanford University in California, says that the β activity that occurs routinely in the motor cortex could be transmitted by the long axons that extend from neurons in this region to the basal ganglia. Also unclear is how the β rhythm interferes with voluntary movement. Starr's group is exploring a phenomenon known as phase–amplitude coupling, which might have an important role in the process. According to this model, the parkinsonian motor cortex is forced to march in lockstep with β rhythms that emanate from the basal ganglia, rather than fire independently to enable normal physical movement.

Make some noise

Against this backdrop, neuroscientists are at a loss as to why DBS works so well. When the rate model prevailed, researchers thought that DBS was directly inhibiting the excessive activity that DeLong, Benabid and their colleagues observed. But researchers have since shown that the electrical stimulation excites rather than inhibits neurons in the basal ganglia, sending neuroscientists back to the drawing board. “We had a situation where subthalamic stimulation was a mainstream therapy that had been done all over the world for ten years with great supporting evidence, but we didn't know how it worked anymore,” says Starr.

“We're taking this pathological behaviour and quashing it.”

Most current pattern-model theories go back to the idea that DBS breaks up the unhealthy rhythms in the motor circuitry by introducing irregular patterns of neuronal activity in the basal ganglia. “We're taking this pathological behaviour and quashing it,” says Lozano. “You seem to be better off with no output than with output that causes trouble.” But researchers are still struggling to understand how this loss of synchronization occurs, and the model is not yet universally accepted.

Whatever the mechanism, the general belief is that the β-band-busting activity of DBS comes from stimulating the cells within the subthalamic nucleus of the basal ganglia. But neuroscientist Gordon Arbuthnott at the Okinawa Institute of Science and Technology in Japan and his colleagues have an alternative theory. They posit that stimulation excites the long axons that connect neurons in the motor cortex with those in the subthalamic nucleus, and that the effect is transmitted 'backwards' along these wires to the motor cortex, rather than 'forwards' into the basal ganglia. The hypothesis is that DBS disrupts unhealthy activity patterns in the motor cortex, and this region, in turn, stops the abnormal synchronization of β activity seen in the basal ganglia^3, 4.

“It seems as though there is a link between motor cortical activity, the loss of β rhythm and recovery,” Arbuthnott says. This would favour a model in which Parkinson's is driven by the motor cortex rather than by the basal ganglia. But research is still at an early stage — the supporting data have mostly come from animal models. Efforts to alleviate Parkinson's symptoms in humans with direct electrical stimulation of the motor cortex, rather than the basal ganglia, have proven disappointing.

A treatment with potential

Unsolved mysteries about the mechanism aside, DBS works — and researchers are now customizing its delivery to individuals through a combination of clinical experience and technological progress.

One of the hot questions concerns when during the course of the disease can DBS do the most good. Most people receive an implant after they have lived with medically managed Parkinson's for more than a decade, when disease progression has made their symptoms more difficult to control. A 2013 clinical trial called EARLYSTIM concluded that intervening a few years earlier might be beneficial⁵. The following year, a pilot study led by researchers at Vanderbilt University in Nashville, Tennessee, went further: they gave DBS to people who had been receiving medication for as little as six months⁶. Both studies provoked a backlash, partly because of the risks associated with neurosurgery, but also owing to fears that such patients might have been misdiagnosed and instead have a different, non-Parkinson's motor disorder.

“After DBS, many people quit their meds and have a very good and stable response.”

But some clinicians believe it is possible to identify those who are most likely to benefit from early intervention. “These are usually patients with early-onset, tremor-dominant Parkinson's disease,” says Bronte-Stewart. After DBS, she says, “many of them quit their meds and have a very good and stable response, and some of them are lucky enough to never develop cognitive impairment.”

At the moment, DBS is an all-or-nothing proposition. It comprises a continuous dose of electrical stimulation at a fixed frequency that can be adjusted only by a specialist. More flexible approaches that are designed to fine-tune the timing, frequency and spatial distribution of the current could both boost the efficacy and reduce the downsides of DBS.

Peter Brown, a neurologist at the University of Oxford, UK, is investigating patterned stimulation. Changing the timing of the electrical pulses can radically alter the effect of DBS on dysfunctional motor-circuit rhythms, he contends: “You can impede them by timing the stimulation appropriately, or you can worsen them by timing it wrong.”

Peter Tass and colleagues at the Jülich Research Centre in Germany are pursuing a version of this approach called coordinated reset, which delivers stimulation sequentially to distinct subpopulations of subthalamic neurons. This approach has shown early promise, and Brown is impressed. “You can treat for a few sessions and there can be this prolonged, sustained improvement for several weeks,” he says.

There are side effects with DBS, such as impaired speech, involuntary movements and cognitive impairment, and these can become especially problematic when stimulation is delivered non-stop. Brown likens it to “heating a room in your house all the time, come summer or winter”. His team is among several that are developing adaptive DBS, in which stimulation changes in response to physiological signals — essentially, installing a thermostat for the brain (see 'Deep brain thermostat'). The hard part is picking the right trigger. Brown's team is focusing on excessive β-band activity in the basal ganglia, and has shown that the adaptive approach delivers symptom relief that is equivalent to conventional DBS, while reducing the side effects⁷. Adaptive systems also consume less power — an important benefit given that standard batteries for current DBS last only 3–4 years and require a surgical procedure to replace.

Meanwhile, Starr's team has identified signatures in the activity of motor-cortex neurons that predict the onset of parkinsonian symptoms, and devised an algorithm that initiates stimulation when these patterns are detected⁸. And Bronte-Stewart's team has developed an adaptive DBS platform that uses Bluetooth-enabled smartwatches to detect the onset of tremor and then signal to the stimulator to respond accordingly⁹.

These adaptive approaches could also help to unlock some mysteries of the parkinsonian brain. Ostrem, for example, has been working with a new DBS system from Medtronic called the Activa PC+S, which allows flexible monitoring of brain activity before, during and after the onset of symptoms. Ostrem notes that these kinds of technologies, combined with accumulating data from high-resolution brain imaging and modelling efforts, could allow treatment regimens that target specific neurological malfunctions. “Parkinson's patients have similar symptoms, but there are probably many reasons why they develop,” she says. “It may be that DBS should not be applied in the exact same way to everyone.”

Although it is important to uncover the mystery of how DBS works, improving the precision of treatment will at least remove some of the urgency from answering such questions.

http://www.nature.com/nature/journal/v538/n7626_supp/full/538S10a.html?WT.mc_id=TWT_OUTLOOK_PD2016

Alzheimer's: Dealing with Difficult Behavior

November 2016  By J B Buckley

As if it weren’t enough to deal with forgetfulness and confusion while caring for your loved-one with Alzheimer’s, but aggressiveness, wandering and paranoia can really put you over the edge. Managing your loved-one’s difficult behavior is your true testament of love and devotion. You know it isn’t their fault, it is their disease that is making them scream, cry or yell terrible things out at you. Who ever said patience is a virtue, didn’t care for a loved-one with Alzheimer’s or dementia. Perhaps a caregiver’s only defense is to understand how to react to difficult behaviors and be ready for them.

Difficult behaviors can be broken down into the following categories: Wandering, Sleeping and Eating Problems, Agitation, Paranoia and difficulty with personal tasks. This is not to say these categories are the only forms of behavioral problems displayed by people living with Alzheimer’s, but their remedies may intersect other problems.

Wandering is not an uncommon hallmark of Alzheimer’s disease or dementia. Stress in the variety of noise, clutter or crowding can cause your loved-one to wander. The best idea is to reduce excess stress. A person living with Alzheimer’s disease should be settled in a quiet, clean, and spacious environment. This will eliminate many of the unwanted stressors, which could cause your loved-one to wander. Other reasons why your loved-one may wander include: Feelings of being lost, boredom, need to use the restroom or medication side effects.

In order to prevent your loved-one from feeling lost or foreign to his or her environment, provide them with familiar objects and reassure them quite frequently that they are at home or in a safe place. Maybe a family photo or an award he or she has won always jogs their memory so keep it close by. If your loved-one displays signs of boredom, give them a task of limited difficulty. This will keep them entertained but won’t frustrate them. Folding laundry is a great activity for people living with Alzheimer’s or dementia.

It is possible that your loved-one is wandering because they need to use the bathroom. In which case, place elaborate signs or pictures on bathroom doors to help guide them. Also, it is a good idea for you to implement regular toilet times. This will keep both of you on schedule. If your loved-one is wandering due to medication side effects, contact their physician to initiate a change in prescription or to lower the dosage. Wandering can be a dangerous behavior. Caregivers should contact their local Alzheimer’s Association to obtain information about ‘The Wanderers Program’ in their area.

People living with Alzheimer’s or dementia often experience sleeping and eating problems. Common causes for these problems include: discomfort, medication, pain, dehydration, depression and excessive sleeping or eating.

Feeling discomfort can sometimes not be conveyed by your loved-one depending upon the severity of the disease but it can cause eating and sleeping disturbances. Frequently monitor your loved-one’s room temperature, lighting, noise level, and chair or bed position. If you think your loved-one’s medications could be curbing his or her appetite or ability to sleep, speak to their doctor about changing or eliminating prescriptions.

Pain can be a factor in eating or sleeping disturbances. Again, sometimes a person with Alzheimer’s or dementia cannot express their feelings; if you sense a change in appetite or sleeping pattern has suddenly occurred without due cause, set an appointment for a medical examination. Dehydration is a known factor of sleeping and eating disturbances. Make sure your loved-one is drinking plenty of water. Place a pitcher filled with water near your loved-one at all times. Remind them it is there frequently and check to make sure it remains somewhat full. Too full can result in another problem- slip and falls.

If you feel your loved-one is showing signs of depression, have him or her evaluated by their physician. Anti-depressants or bedtime sedatives may be a productive treatment option. Depression can also cause excessive sleeping or eating. In which case, increase their exposure to light and reduce or eliminate nap time or snack time.

Defined:
Behavioral problems are defined as patient responses, which are considered noxious to staff, other patients, the patient himself, or family (Burgio, Jones, Butler, & Engel, l988). Behavioral problems have a profound impact on quality of care, staff, morale and the day-to-day operation of the long-term care institution

http://www.caregiver.com/channels/alz/articles/alzheimers_difficult_behavior.htm

Alzheimer's: Eye test may predict if you'll develop the disease, research suggests

November 11, 2016

A simple eye test could determine if a person is likely to develop Alzheimer's disease decades before they show symptoms, a leading US medical scientist says.

Professor Peter Snyder, a neuroscientist from Brown University and Rhode Island Hospital in the US, said the presence of retinal plaque on a person's eyes could be a precursor to determine whether someone will develop the disease.

He is visiting Griffith University on Queensland's Gold Coast and will present his findings to a conference this weekend.

He said early research had been promising, but a diagnostic technology was still several years away.

"What I'm looking for are tiny, tiny inclusion bodies or plaques in the retina that seem to correlate with the amount of amyloid protein built up in the brain," Professor Snyder said.

"By the time someone has symptoms, if the disease has been creeping up in the brain for 20 or 30 years, by the time they are showing symptoms, it may already be too late.

"It's very hard to save tissue that is already dead or dying, so I want to identify people early so that we can develop effective therapies."

Professor Snyder's research included testing 80 people with an average age of 61, and giving them brain scans.

Of those people, 20 had a build up of amyloid protein in the brain, which was already a confirmed identifier of Alzheimer's disease, and almost all of those 20 people had signs of retinal plaque.

'I do worry' about people finding out early

Professor Snyder said he understood some people might not want to know if they were likely to develop Alzheimer's.

"These people [who test positive] are still ostensibly healthy," he said.

"They're raising families and sending kids off to college and going to work and I do worry about this.

"It really is a chicken and egg issue, but I honestly believe that if we don't try to test drugs, therapies that might be effective in people in the earliest stages of the disease we're never going to find something that slows progression of the disease."

He said he found that once people realised they were at an increased risk, they looked after themselves better, but people who were found not at risk, did not.

"There's an amazing thing that happens — they start to take better care of themselves, they start to eat a healthier diet, they start to exercise more, they start to improve their sleep habits.

"And the funny thing is the people who know they're low risk, do none of those things to improve their health, so there may actually be a silver lining to this."

http://www.abc.net.au/news/2016-11-11/alzheimers-disease-eye-test-could-predict-development-of-disease/8016072

It’s all in your head: Pitt researchers measure hallucinations

November 10, 2016  James Evan Bowen-Gaddy 

When you think of hallucinations, you may think of a woozy feeling and swimming images or of the bright spots you see after rubbing your eyes.

Hallucinations are typically an undesired side effect of sleep deprivation, mental illness or certain prescription drugs –– called psychotropics –– but there are few ways to accurately study and measure them.

So one team of Pitt researchers gave a group of people basic hallucinations on purpose, then mapped out how their brains responded.

Bard Ermentrout of the University of Pittsburgh –– a computational biology researcher –– along with Joel Pearson of the University of South Wales and a team of four other researchers, announced in October that they were able to measure and objectively study the mental mechanisms behind hallucinations.

By inducing visual hallucinations in otherwise healthy individuals, the researchers made progress toward explaining and understanding disease-induced hallucinations, such as ones caused by Parkinson’s disease, schizophrenia and epilepsy. 

To complete their study, the team induced simple hallucinations in healthy subjects by flickering high-frequency light, and then asked the subjects to compare what they saw against a physical stimulus. 

“We can use flicker to study the general mechanisms of hallucinations with anybody, anytime. That means we don’t have to rely on recruiting unwell people and clinical populations,” Pearson said.

This research was a step toward being able to study the visual hallucinations associated with Parkinson’s disease, according to Pearson. For patients with Parkinson’s disease, the visual hallucinations can be debilitating, in part because it’s difficult to predict when they might strike. 

Pearson said these hallucinations are also difficult to objectively quantify –– a crucial first step in scientific research –– so his most recent study opens avenues to investigate these phenomena without inconveniencing people afflicted by the disease.

The study used a well-known method of flicker-induced hallucinations, in which the researcher exposes a subject to a bright, flickering computer monitor until the subject begins to see shapes that are not there. Changing the frequency of these flickers can change the kinds of patterns subjects see.

Then Pearson and Ermentrout added their own spin. Instead of using a large flickering screen, which produces hallucinations of multiple shapes and colors, the researchers reduced the flickering space to a small ring shape. Pearson said this reduces the possibilities of hallucinations down to simple gray blobs that rotate around the ring in seemingly random directions. 

In natural circumstances, hallucinations are a subjective experience, varying widely from person to person. A researcher, however, can’t make sense of hallucinations in a lab setting if those hallucinations are spontaneous and individualized.

By simplifying the hallucinations down to simple blobs, the research team minimized the subjectivity of the experiment and created hallucinations that were relatively consistent from one subject to the next. 

“To do good science, we needed a simple shape,” Pearson said.

In order to study the simple hallucinations objectively, the team placed another smaller ring within the flickering one, which housed actual images of gray blobs, in addition to the hallucinated blobs. Pearson said subjects told researchers whether the hallucinated blobs were more or less pronounced than the actual images of blobs. This method of comparison allowed the team to make objective and consistent measurements, instead of relying on subjective accounts from each study participant.

“This lets us do a very basic experiment where we can see at what point people are equally likely to say the perceptual and the hallucinated blobs are the same strength,” Pearson said. “That gives us the first reliable measure of the hallucination strength.” 

Ermentrout then focused most of his effort throughout the study on producing a mathematical “map” of the visual cortex during a hallucination of simple blobs. The “maps” show how the ring and hallucinated blobs appear on tissue in the visual cortex. 

Ermentrout –– who has been modeling the brain since 1979 when he developed a mathematical theory of how the brain reacts to mescaline –– said his recent study made sense of the instabilities that arise in the brain during a hallucination.

“Now we can build up a real quantitative idea of how these hallucinations are formed,” Ermentrout said. 

Stewart Heitmann –– who conducted postdoctoral research with Ermentrout and is a current member of the hallucination research team –– said this kind of mathematical modeling of the brain is important to developing a better understanding of visual hallucinations.

“The main claim of the paper is that an objective measure has been made of a subjective experience,” Heitmann said. “If it can glean a better understanding on [the brain’s] architecture, it gives you a better understanding of how the visual cortex works.”

The team plans to continue researching hallucinations, looking to further compare their models against quantitative data. Their major obstacle is the chaotic and personal nature of hallucinations.

“Here’s the tricky thing with science. We need something reliable to scientifically study it,” Pearson said.

http://pittnews.com/article/113699/top-stories/pitt-researchers-measure-hallucinations/

Caring for veterans: A privilege and a duty

GOD BLESS EVERY VETERAN!

November 10, 2016

In this April 2, 2015, file photo, a visitor leaves the Sacramento Veterans Affairs Medical Center in Rancho Cordova, California

Veterans Day had its start as Armistice Day, marking the end of World War I hostilities. The holiday serves as an occasion to both honor those who have served in our armed forces and to ask whether we, as a nation, are doing right by them. 

In recent years, that question has been directed most urgently at Veterans Affairs hospitals. Some critics are even calling for the dismantling of the whole huge system of hospitals and outpatient clinics. 

President Obama signed a US$16 billion dollar bill to reduce wait times in 2014 to do things like hire more medical staff and open more facilities. And while progress has been made, much remains to be done. The system needs to improve access and timeliness of care, reduce often challenging bureaucratic hurdles and pay more attention to what front-line clinicians need to perform their duties well. There is no question that the VA health care system has to change, and it already has begun this process.

Over the past 25 years, I have been a medical student, chief resident, research fellow and practicing physician at four different VA hospitals. My research has led me to spend time in more than a dozen additional VA medical centers. 

I know how VA hospitals work, and often have a hard time recognizing them as portrayed in today’s political and media environment. My experience is that the VA hospitals I know provide high-quality, compassionate care. 

Treating nine million veterans a year

I don’t think most people have any sense of the size and scope of the VA system. Its 168 medical centers and more than one thousand outpatient clinics and other facilities serve almost nine million veterans a year, making it the largest integrated health care system in the country. 

And many Americans may not know the role VA hospitals play in medical education. Two out of three medical doctors in practice in the U.S. today received some part of their training at a VA hospital. 

The reason dates to the end of World War II. The VA faced a physician shortage, as almost 16 million Americans returned from war, many needing health care. 

At the same time, many doctors returned from World War II and needed to complete their residency training. The VA and the nation’s medical schools thus became partners. In fact, the VA is the largest provider of health care training in the country, which increases the likelihood that trainees will consider working for the VA once they finish.

Michael Storemski talks with Dr. Christina Henson following his treatment at the Veterans Administration Medical Center in Oklahoma City in June 2014.

Specialized care for veterans

The VA network specializes in the treatment of such war-related problems as post-traumatic stress disorder and suicide prevention. It has, for example, pioneered the integration of primary care with mental health. 

Many veterans live in rural parts of the U.S., are of advanced age and have chronic medical conditions that make travel challenging. So the VA is a national leader in telemedicine, with notable success in mental health care. 

The VA’s research programs have made major breakthroughs in areas such as cardiac care, prosthetics and infection prevention. 

I can vouch for the VA’s nationwide electronic medical records system, which for many years was at the cutting edge. 

A case in point: Several years ago a veteran, in the middle of a cross-country trip, was driving through Michigan when he began feeling sick. Within minutes of his arrival at our VA hospital, we were able to access his records from a VA medical center over a thousand miles away, learn that he had a history of Addison disease, a rare condition, and provide prompt treatment.

I am therefore not surprised that the studies that have compared VA with non-VA care have found that the VA is, overall, as good as or better than the private sector. In fact, a recently published systematic review of 69 studies performed by RAND investigators concluded: “…the available data indicate overall comparable health care quality in VA facilities compared to non-VA facilities with regard to safety and effectiveness.”

Optometrist Paul Archambault, left, talks with U.S. Army veteran Kenneth Chavis during a glaucoma examination at the Fayetteville Veterans Affairs Medical Center in Fayetteville, N.C. 

The VA offers veterans more than health care

The most remarkable aspect of VA hospitals, though, is the patient population, the men and women who have sacrificed for their country. They have a common bond. A patient explained it this way:

“The VA is different because everyone has done something similar, whether you were in World War II or Korea or Nam, like me. You’re not thrown into a pot with other people, which would happen at another kind of hospital.”

The people who work at VA hospitals have a special attitude toward their patients. It takes the form of respect and gratitude, of empathy, of a level of caring that is nothing short of love. You can see it in the extra services provided for patients who are often alone in the world, or too far from home to be visited.

Take a familiar scene: a medical student taking a patient for a walk or wheelchair ride on the hospital grounds. It is common for nurses to say “our veteran” when discussing a patient’s care with me.

Volunteers and chaplains rotate through VA hospitals on a regular basis, to a degree unknown in most community hospitals. The social work department is also more active. The patients are not always so patient, but these visitors persevere. “They’re a good bunch of people,” one veteran said of the staff. “I know because I’m irritable most of the time and they all get along with me.”

Physicians everywhere are under heavy pressure these days, in part because of the increase in the number of complex patients they care for. Yet I have spent hours observing doctors in VA hospitals around the country as they sit with patients, inquiring about their families and their military service, treating the veterans with respect and without haste.

Earlier this year, I cared for a veteran in his 50’s, a house painter, whom we diagnosed with cancer that had metastasized widely. We offered him chemotherapy, which could have given him an extra few months, but he chose hospice. He told me he wanted to go home to be with his wife and play the guitar. One of the songs he wanted to sing was “Knocking on Heaven’s Door.”

I was deeply moved. I liked and admired the man, and I was disturbed that we had been unable to save him. My medical student had the same feelings. Before the patient left, the student told me, “He shook my hand, looked me in the eyes, and said, ‘Thanks for being a warrior for me.’”

That’s the special kind of patient who shows up at a VA hospital. Every single one of them should have the special kind of care they deserve. And we must ensure that the care is superb on this and every day.

https://theconversation.com/caring-for-veterans-a-privilege-and-a-duty-67823