Illnesses/diseases Recognized by the VA as connected to agent orange herbicide exposure

Causes from agent orange:

acute peripheral neuropathy: a tempo- rary dysfunction of the nervous system characterized by involuntary “tingling” or numbness in the extremities adult onset type II diabetes Mellitus (and subsequent complications caused by): non-insulin dependent and charac- terized by high blood sugars al amyloidosis: a rare group of diseases that results from the abnormal deposition of a particular protein called amyloid in various tissues of the body *chloracne: an acne-like eruption on the skin due to prolonged exposure to certain chlorinated compounds hodgkins disease: a tumor found in the lymph nodes characterized by increas- ing enlargement of the lymph nodes, liver, and spleen, and accompanied by progressive anemia Ischemic (or ischaemic) heart disease: a heart condition resulting when the arteries that bring blood and oxygen to the heart are blocked. There may be a buildup of cholesterol and other sub- stances, called plaque, in the arteries that bring oxygen to heart muscle tis- sue. Over time, the heart muscle does not work well, and it is more difficult for the heart to fill and release blood. It is the most common cause of congestive heart failure. non-hodgkins lymphoma: Non-Hodg- kins lymphoma, including chronic lymphocytic leukemia and small-cell lymphocytic lymphoma: a rare type of cancer which causes malignant tumors of the lymph nodes, distinguished from Hodgkins disease by the absence of giant Reed-Sternberg cells. parkinson’s disease: a neurological disease limiting the ability to control some muscles. Caused by a gradual loss of dopamine-manufacturing cells in the brain, Parkinson’s disease often causes movement and muscle problems and may be accompanied by slight, uncontrolled shaking of the arms and legs. *peripheral neuropathy: a dysfunction of the nervous system involving either the somatic nerves or the autonomic nervous system (see Acute Peripheral Neuropathy); can cause sensory loss, atrophy, and muscle weakness *porphyria cutanea tarda: characterized by skin lesions on exposed portions of the body and pigment changes in the skin; liver disease occurs in some patients spina bifida in children conceived after the veteran first arrived in Vietnam: characterized by a defective closure of the spinal cord in which the cord may be exposed and/or protrude sub-acute peripheral neuropathy: a nervous system disorder either acute (temporary) or chronic (long-term) – see acute peripheral neuropathy and peripheral neuropathy cancers cancer of the bronchus: a malignant tumor found in the bronchus, an extension of the windpipe (trachea) connecting to the lungs cancer of the larynx: a malignant tu- mor found in the voice box (larynx) cancer of the lung: a malignant tumor found in the lungs cancer of the prostate: a malignant tumor found in the prostate gland cancer of the trachea: a malignant tumor found in the windpipe (trachea) adult Fibrosarcoma: a tumor formed from connective tissue alveolar soft part sarcoma: a sarcoma found in the aveoli, the sac-like ducts in the lungs angiosarcoma: a tumor occurring on the breast and skin and believed to originate from blood vessels chronic lymphocytic leukemia: char- acterized by a progressive increase in production of white blood cells clear cell sarcoma of aponeuroses: a sarcoma found at the end of a muscle where it becomes a tendon clear cell sarcoma of tendons: a sarcoma found in the tendons congenital Fibrosarcoma: a malignant tumor formed before birth and derived from connective tissue dermatofibrosarcoma: a relatively slow- growing skin tumor consisting of one or more firm nodules ectomesenchymoma: a tumor found in certain parts of the skin epithelioid Malignant leiomysarcoma: a malignant tumor derived from smooth muscle found in the layer covering the muscle epithelioid Malignant schwannoma: a moderately firm, benign tumor found in the layers of membrane covering surfaces inside the body cavity caused by too many Schwann cells growing in a disorderly manner epithelioid sarcoma: a tumor found in the membrane covering surfaces inside the body cavity extraskeletal ewing’s sarcoma: a tumor outside the bone consisting of small rounded cells

SERVICE-CONNECTED DISABIlITY COMPENSATION FOR EXPOSURE TO AGENT ORANGE 4

hairy cell leukemia: a rare slow- growing chronic cancer of the blood called such because the leukemic lymphocytes have short, thin projec- tions on their surfaces that look

like hairs when examined under a microscope. Hairy cell leukemia is caused by an abnormal change in B lymphocytes (a type of white cell).

hemangiosarcoma: a tumor derived from blood vessels and lining blood- filled spaces

Infantile Fibrosarcoma: a tumor formed as a child derived from fibrous connective tissue

leiomyosarcoma: a tumor derived from smooth muscle

liposarcoma: a tumor that may occur anywhere in the body consisting of irregular fat cells

lymphangiosarcoma: a tumor derived from blood vessels

lymphoma: a malignant tumor of the lymph nodes

Malignant Fibrous histiocytoma: a type of tumor found in connective tissue

Malignant giant cell tumor of the tendon sheath: a tumor found in the membrane of tendons

Malignant glandular schwannoma:
a moderately firm malignant tumor
in the glands caused by too many Schwann cells growing in a disorderly pattern

Malignant glomus tumor: a tumor found in the tiny nodes (glomuli) in the the nailbed, pads of fingers, toes, ears, hands, feet, and other body organs

Malignant hemangiopericytoma: a tumor characterized by rapidly growing fat cells formed in blood vessels and lining blood-filled spaces

Malignant Mesenchymoma: a malig- nant tumor in the embryonic tissue or fluid

Malignant shwannoma with Rhabdo- myoblastic: a moderately firm malig- nant tumor found in skeletal muscle resulting from the rapid disorderly growth pattern of Schwann cells

Multiple Myeloma: cancer of specific bone marrow cells characterized by bone marrow tumors in the skeletal system

Proliferating angiedotheliomatosis: increasing numbers of benign tumors in blood cells often causing skin discoloration

Rhabdomysarcoma: tumors derived from skeletal muscle

Sarcoma: tumors arising in connec- tive tissue, bone, cartilage, or muscle
soft tissue sarcoma: a group of soft tissue cancers characterized by malignant tumors which develop on muscles and connective tissue, or in body fat

Synovial sarcoma: a tumor found in the lubricating fluid surrounding joints and tendons

* Diseases with various time requirements A current version of this guide can be
viewed online at www.vva.org.
Note: this list may change over time. For official updates, see title 38 Code of Federal Regulations Section 3.309(e) “Diseases associated with exposure to certain herbicide agents.”

BIRTH Defects RecognIzed by the VA as connected to Agent Orange Exposure

Spina bifida: children born to either male or female Vietnam veterans;  Spina Bifida Occulta not included children born to Female Vietnam Veterans achondroplasia: produces a type of dwarfism cleft lip and cleft palate congenital heart disease congenital talipses equinovarus: clubfoot esophageal and Intestinal atresia hallerman-streiff syndrome: premature small growth and other related defects hip dysplasia hirschprung’s disease: congenital megacolon hydrocephalus due to aqueductal stenosis hypospadias: abnormal opening in the urethra Imperforate anus neural tube defects Poland syndrome: webbed fingers Pyloric stenosis syndactyly: fused digits tracheoesophageal Fistula Undescended testicles Williams syndrome: thyroid defects Not covered are conditions that are congenital malignant neoplasms, chromosomal disorders, or developmental disorders. In addition, condi- tions that do not result in permanent physical or mental disability are not covered. Note: this list may change over time. Veterans may obtain more information on birth defects and should register all children and grandchildren with birth defects, including cancers and learning disabilities, online at www.birthdefects.org, main- tained by the National Birth Defect Registry.

Is Modern living leading to a ‘hidden epidemic’ of neurological disease?

Date:

August 6, 2015

Source:

Bournemouth University

Summary:

Modern living could be responsible for an 'almost epidemic' increase in neurological brain disease.

Modern living could be responsible for an 'almost epidemic' increase in neurological brain disease, according to new research from Bournemouth University.

Published in the journal Surgical Neurology International the study compared 21 Western countries between 1989 and 2010 and found that dementias are starting a decade earlier than they used to in adults.

Furthermore deaths caused by neurological disease have risen significantly in adults aged 55-74, and for adults 75+ the rate has virtually doubled in every Western country in just the last 20 years.

In the US, the problem is particularly acute; neurological deaths in male over 75s have nearly trebled and females rose more than five-fold.

For the first time since records began, more elderly US women died of brain disease than cancer.

Professor Colin Pritchard of Bournemouth University led the study said "The rate of increase in such a short time suggests a silent or even a `hidden' epidemic, in which environmental factors must play a major part, not just aging. Modern living produces multi-interactional environmental pollution but the changes in human morbidity, including neurological disease is remarkable and points to environmental influences."

Professor Prichard continued, "Furthermore are the practical implications for families trying to cope as front-line services are being swamped. For example, the remarkable increase in Motor Neuron Disease in the UK, as well as the earlier dementias. Exemplified in a new charity `Young Dementia UK, who report that many of their clients are in their late 40's and early 50's- something unthinkable twenty years ago"

"In part, some of the results are explained by more effective treatments for cancer and heart disease, with advances in medicine making such physical illnesses easier to treat, whilst there have been less advances in the treatment of neurological conditions"

"Crucially it is not just because people are living longer to get diseases they previously would not have lived long enough to develop but older people are developing neurological disease more than ever before.

The environmental changes in the last 20 years have seen increases in the human environment of petro-chemicals -- air transport- quadrupling of motor vehicles, insecticides and rises in background electro-magnetic-field, and so on."

"These results will not be welcome news as there are many with short-term vested interests that will want to ignore them. It is not that we want to stop the modern world but rather make it safer.

Essentially, it is time for us to wake up and realize that a major problem we now face is unprecedented levels of neurological disease, not just the earlier dementias and thinking of the USA -- `when America sneezes, Europe gets cold a decade later."

Journal Reference:
Colin Pritchard, Emily Rosenorn-Lanng. Neurological deaths of American adults (55-74) and the over 75′s by sex compared with 20 Western countries 1989-2010: Cause for concern. Surgical Neurology International, 2015; 6 (1): 123 DOI: 10.4103/2152-7806.161420

Bournemouth University. "Is Modern living leading to a ‘hidden epidemic’ of neurological disease?." 
ScienceDaily. ScienceDaily, 6 August 2015.
 <www.sciencedaily.com/releases/2015/08/150806091328.htm>.

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Will Parkinson's Change How I'm Seen as a Dad

FoxFeed Blog

Posted by  Bryan Roberts, August 07, 2015

Bryan M. Roberts, Associate Dean at the Roy H. Park School of Communications at Ithaca College and member of the MJFF Patient Council, blogs at Stepping Forward: Life with Young Onset Parkinson's Disease. He shares his light-hearted reflection on being a dad with Young-onset Parkinson's disease.

I tend to take very few things in life seriously — including my own health. One of the only things that I'm truly dedicated to is being a good father. This also gives me a large amount of anxiety — will my daughter see me as being "sick"? Will it diminish her childhood in significant ways? Make her feel that she received a raw deal in the "parent lottery"? Will this feeling engender low self-esteem and lead to poor life decisions — like dating a NBA player with a neck tattoo, becoming one of those idiots who enjoys the World Cup or, sweet Jesus, enrolling at Syracuse University?

This has been weighing heavily on my mind recently as Avery turns four. I have had Parkinson's for her entire life. She'll never know Bryan Roberts: the guy who was a stud athlete; Bryan Roberts: the guy who never got sick; Bryan Roberts: the guy who almost chose military service over college; Bryan Roberts: the guy who dated the underwear model with shaky moral values (she is probably better off not knowing about this), etc.

Then I found myself at a Michael J. Fox Foundation fundraiser standing next to Michael's son, Sam (not to be confused with the other Sam Fox who runs long distances and climbs mountains for sport). We got to talking and after a while of discussion, started talking about raising kids while having PD. I disclosed my fear of seriously messing her up and then Sam put my mind at ease. He said:

"Growing up it wasn't dad who has Parkinson's disease. Dad is just dad."

That simple phrase really put things in perspective. My daughter won't know what I was or what I am not, she will just know that I'm her father and I love her very much. Parkinson's disease may be a disease of diminishment but it doesn't have to be. Some roles, like a parent, are too big to be diminished.

So, happy birthday, Young Roberts — your dad loves you and is incredibly proud of you.

https://www.michaeljfox.org/foundation/news-detail.php?will-parkinson-change-how-seen-as-dad&os_cid=fb-a30U00000004hJs&s_src=MJFFfb&s_subsrc=bryanroberts_dad#prclt-Nh819TPP

New Techniques To Move Patients Improve Safety

                                       New Techniques To Move Patients Improve Safety
Click on to :
https://youtu.be/SCXJUFI0lGc

Parkinson's May Spread From Gut to Brain via Vagus Nerve

Megan Brooks

August 06, 2015

A large Danish epidemiologic study supports the theory that Parkinson's disease (PD) may begin in the gastrointestinal tract and spread through the vagus nerve to the brain. Researchers found that patients who have had the entire vagus nerve severed were less apt to develop PD.

"Their risk was halved after 20 years," Elisabeth Svensson, PhD, from the Department of Clinical Epidemiology, Aarhus University in Denmark, said in a statement.

"However, patients who had only had a small part of the vagus nerve severed were not protected. This also fits the hypothesis that the disease process is strongly dependent on a fully or partially intact vagus nerve to be able to reach and affect the brain," Dr Svensson noted.

This study is an "important piece of the puzzle" in terms of the causes of PD, she told Medscape Medical News.

The study was published online July 17 in Annals of Neurology.

Gut-Brain Connection in PD

In the past, vagotomy was commonly performed for peptic ulcer, the researchers note in their paper. The two most common procedures were full truncal vagotomy, in which both vagal trunks were severed, and superselective vagotomy, in which only the nerves supplying the fundus and body of the stomach were resected.

Using prospectively collected Danish registry data, the researchers investigated the risk for PD in 5339 patients who had truncal and 5870 who had superselective vagotomy, in relation to 66,711 and 60,500 matched population controls, respectively.

A direct comparison of the two vagotomy groups showed that patients who had truncal vagotomy had a lower risk for PD than did those having the superselective procedure, after adjustment for age and sex (adjusted hazard ratio [HR], 0.85; 95% confidence interval [CI], 0.56 - 1.27). After a follow-up period of over 20 years after the date of surgery, the age- and sex-adjusted HR was 0.58 (95% CI, 0.28 - 1.20), the researchers report.

The risk for PD was also lower after truncal vagotomy when compared with the general population. The overall adjusted HR was 0.84 (95% CI, 0.63 - 1.14). After more than 20 years' follow-up, the adjusted HR was 0.53 (95% CI, 0.28 - 0.99).

The risk for PD in patients who had superselective vagotomy was similar to that in population controls overall (HR, 1.09; 95% CI, 0.84 - 1.43) and after 20 years (HR, 1.16; 95% CI, 0.80 - 1.70).

These findings, say the researchers, "suggest that having an intact vagus nerve increases the risk of developing PD. The finding is in accord with a primary pathological process being initiated in the gastrointestinal mucosa, which then uses the vagus as a major entry point into the brain."

They say strengths of the study include the large sample size and nationwide population-based design with long-term follow-up, reducing the potential for selection bias. They note, however, that the statistical precision of their risk estimates was "limited" and they encourage independent verification of their observations.

Important Contribution

Christopher H. Hawkes, MD, FRCP, professor of neurology, Barts and the London School of Medicine & Dentistry, United Kingdom, who reviewed the findings for Medscape Medical News, called them "very interesting."

He noted that while the article is "awash with adjustments, nonsignificant results and unfamiliar statistical methods," the conclusion is "plausible, particularly the 35-year cumulative PD incidence curve that shows a clear diverging separation of the total vagotomy group compared to the general population. The beneficial effect size of surgery is difficult to quantify but likely to be small, eg, not more than a 1% lower risk for those who had truncal vagotomy."

Dr Hawkes said the findings "support the original proposal by Braak et al. who suggested that a neuropathogen, present in the gastric mucosa, traveled up vagal afferent fibers, resulting in Lewy-related pathology in the dorsal motor nucleus of the vagus and glossopharyngeal nerves. Also supported is the concept of a prolonged prodrome, given that the cumulative curve is divergent even after 35 years."

"Overall, this is an important contribution to our understanding of PD that reinforces the concept of a transmissible neurotropic agent," Dr Hawkes concluded.

The study was funded by the Program for Clinical Research Infrastructure established by the Lundbeck and Novo Nordisk Foundations, the Aarhus University Research Foundation, and the Danish Parkinson Foundation. The authors and Dr Hawkes have disclosed no relevant financial relationships.

Ann Neurol. Published online July 17, 2015. Abstract

http://www.medscape.com/viewarticle/849140?src=wnl_edit_tpal

Disability Benefits Extended to Air Force, Reserve Personnel Who Were Exposed to Agent Orange

Posted: Aug 05, 2015 3:55 AM EDTUpdated: Aug 07, 2015 1:54 PM EDT

Over 2,000 service members may be eligible for benefits after exposure to herbicide in Vietnam

This article was originally distributed via 24-7 Press Release Newswire. 24-7 Press Release Newswire, WorldNow and this Site make no warranties or representations in connection therewith.

WASHINGTON, DC, August 05, 2015 /24-7PressRelease/ -- A new group of veterans became eligible Friday for disability benefits covering treatment of conditions tied to Agent Orange exposure. According to a news release issued by the Department of Veterans Affairs (VA), the benefits will be available to an estimated 1,500 to 2,100 service members who were part of the Air Force and Air Force Reserve during the Vietnam War. 

The Air Force personnel and reservists suspected of exposure to Agent Orange acted as flight, ground and medical crew members on C-123 aircraft used to disperse the herbicide during the Vietnam War. The VA has identified 14 conditions associated with Agent Orange exposure, including Parkinson's disease, type 2 diabetes and multiple forms of cancer. 

"The VA's decision to extend benefits eligibility to these veterans is the right thing to do," said Vanessa Brice, a veterans' benefits attorney with the Orlando law firm of Colling Gilbert Wright & Carter. "These men risked their lives for our country, and now that decades have passed and we know about the devastating consequences of Agent Orange exposure, the government has a duty to make adequate compensation available." 

According to The New York Times, this decision marks the first time the VA has extended disability benefits for Agent Orange exposure to service members who weren't deployed on land or inland bodies of water during the Vietnam War. An estimated $47.5 million is expected to be set aside over the next 10 years.

Unfortunately, service members who are now eligible for disability benefits to cover the cost of treatment for diseases tied to Agent Orange aren't automatically guaranteed the compensation they deserve, Brice said. 

"The application for VA benefits is very strict, and many deserving veterans have their claims denied," she said. "An experienced attorney can review a serviceman or servicewoman's medical records and provide support throughout the appeals process."

About Colling Gilbert Wright & Carter

Founded in 2005, Colling Gilbert Wright & Carter is a plaintiffs' personal injury law firm representing clients in Orlando, the state of Florida and nationwide. Attorneys at the firm also have experience launching appeals on behalf of veterans of the U.S. military whose disability benefits claims were denied by the Department of Veterans Affairs. For more information, please visit www.thefloridafirm.com

Information contained on this page is provided by an independent third-party content provider. WorldNow and this Station make no warranties or representations in connection therewith. If you have any questions or comments about this page please contact pressreleases@worldnow.com.

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http://world.einnews.com/article/279970766/3lyqCntkcz5LjS0L

Could sleeping on your side reduce the risk of developing Alzheimer’s and Parkinson’s disease?

Aug 5, 2015 at 9:25 AM

We’ve been told that our sleep positions clearly plays a role when it comes to neck or back pain, but researchers have found that it could actually affect our brains and our risk for disease.

A team at Stony Brook University used MRI scans to image the brain’s glymphatic pathway, the complex system that clears wastes and other harmful chemical solutes from the brain. What they found is that the brain does a better job of clearing out this waste when we sleep laterally, on our sides. This could actually play a role in decreasing the chances of developing neurological diseases like Alzheimer’s and Parkinson’s.

Dr. Helene Benveniste, principal investigator and a professor in the departments of anesthesiology and radiology at Stony Brook University, and her colleagues looked at anesthetized rodents and used a dynamic contrast MRI method to monitor the functioning glymphatic pathway in anesthetized rodents’ brains in three positions – lateral (side), prone (down), and supine (up).“The analysis showed us consistently that glymphatic transport was most efficient in the lateral position when compared to the supine or prone positions,” said Dr. Benveniste, according to a press release. “Because of this finding, we propose that the body posture and sleep quality should be considered when standardizing future diagnostic imaging procedures to assess CSF-ISF transport in humans and therefore the assessment of the  of damaging brain proteins that may contribute to or cause brain diseases.”

The CSF-ISF transport she mentions refers to the process when cerebrospinal fluid (CSF) filters through the brain and exchanges with interstitial fluid (ISF) to clear waste, similar to the way the body’s lymphatic system clears waste from organs.

Maiken Nedergaard, PhD is one member of the team that contributed from the University of Rochester. She had this to say about their findings:

“It is interesting that the lateral sleep position is already the most popular in human and most animals – even in the wild – and it appears that we have adapted the lateral sleep position to most efficiently clear our brain of the metabolic waste products that built up while we are awake,” says Dr. Nedergaard. “The study therefore adds further support to the concept that sleep subserves a distinct biological function of sleep and that is to ‘clean up’ the mess that accumulates while we are awake. Many types of dementia are linked to sleep disturbances, including difficulties in falling asleep. It is increasing acknowledged that these sleep disturbances may accelerate memory loss in Alzheimer’s disease. Our finding brings new insight into this topic by showing it is also important what position you sleep in.”

Clearly it will be important to do the same kind of testing on humans, but the researchers believe the results will be similar to that in the rodents.

http://medcitynews.com/2015/08/sleep-positions-postures-alzheimers-parkinsons-neurology/?utm_source=MedCity+News+Subscribers&utm_campaign=b80e7cdaff-RSS_EMAIL_CAMPAIGN&utm_medium=email&utm_term=0_c05cce483a-b80e7cdaff-67807189

How the finch changes its tune has implications for humans

Published: Tuesday 4 August 2015 at 3am PST

UCSF researchers discover mechanism for learning in adult songbirds

Like top musicians, songbirds train from a young age to weed out errors and trim variability from their songs, ultimately becoming consistent and reliable performers. But as with human musicians, even the best are not machines. To learn and improve, the songbird brain needs to shake up its tried-and-true patterns with a healthy dose of creative experimentation. Until now, no one has found a specific mechanism by which this could occur.

Now, researchers at UC San Francisco have discovered a neurological mechanism that could explain how songbirds' neural creativity-generator lets them refine and alter their songs as adults. The finding could help explain how the human brain learns complex motor skills - from playing the oboe to driving a car - and may have long-term implications for treating neurological conditions ranging from Parkinson's disease to obsessive disorders.

To learn its song, a bird uses a specialized portion of its brain equivalent to the human basal ganglia, a collection of neural structures nestled in the base of the brain.

"This is an incredibly well conserved circuit - from lampreys to us - which in humans is connected to everything from movement to mood," said lead author Hamish Mehaffey, PhD, a post-doctoral researcher in the lab of the late Allison Doupe, MD, PhD, a beloved professor of psychiatry and psychology at UCSF who passed away in October 2014.

In her 20 years at UCSF, Doupe established the birdsong system as a model for the basal ganglia's role in human language, fine motor learning and psychiatric disease, said Michael Brainard, PhD, a UCSF professor of physiology who was both Doupe's husband and a frequent collaborator.

"Her recent work had shown that precise patterns of activity arising from the basal ganglia were important for brain plasticity and learning, but we didn't understand what aspects of that patterning were important," Brainard said. "The current results demonstrate a mechanism that could explain why these activity patterns matter and reveal the 'rules' that let them alter brain connectivity. This is a key advance."

Young male zebra finches spend their lives perfecting their boisterous mating song, which sounds a bit like a droid from Star Wars. Young birds learn by trial and error to produce an accurate cover of their father's mating song, but as adults they are not above tweaking a phrase or two in their efforts to impress potential mates, or as needed to adjust their technique for growth, age or injury.

Doupe's previous research revealed that the avian equivalent of the human basal ganglia plays a crucial role in the creative experimentation required for song learning. When researchers block the output of the basal ganglia, young birds never develop a mature song, and adults lose the ability to adjust and maintain their song based on experience.

Doupe's work also found that the creativity engine of the basal ganglia is more active when birds practice their songs alone, injecting variability into the song motor circuit to let the birds try out new notes and modified motifs. But when a pretty female shows up, the researchers found, the creativity circuit shuts down to let the bird reliably produce the best, most tried-and-true version of its song. The basal ganglia also are needed to lock in any change to a new part of the song that the bird is practicing.

Researchers trying to understand how the basal ganglia's instructive signals enable trial-and-error learning have been perplexed by their unpredictable timing. Unlike the brain region that acts as a conductor for the bird's song, which issues bursts of activity precisely timed to initiate specific notes and motifs, the timing of the basal ganglia's signals, when they chime in at all, is off-beat and hard to predict.

"On the one hand, if there's no variability, there's no trial-and-error learning," said Mehaffey. "If the bird can't explore, it will never find a better version of its song. On the other hand, this variability has confused a lot of us, because if the bird needs to modify a specific note's pitch, the signal needs to be very precisely timed."

The new paper, which appeared online August 3, 2015 in the journal Nature Neuroscience, is the first to examine in detail the synapse-level learning rules that could allow the basal ganglia's variable signals to modify the motor plan controlling the bird's song.

Using brain slices containing the region where inputs from the basal ganglia and the song motor pathway converge to control the bird's song performance, Mehaffey electrically stimulated the two pathways to show that the relative timing of their signals - one for "creativity" and the other encoding the established song - can lead to synaptic changes that either put the basal ganglia temporarily in the driver's seat or hand the reins back to the learned motor plan.

Further research in live animals suggested that the same synaptic learning mechanism may be necessary for adult birds to modify their songs based on experience. The scientists exposed birds to an irritating burst of static tied to the pitch of a specific note in their songs. Typically, birds quickly learn to modify this note to avoid the burst of noise, but when the researchers gave the birds a drug that specifically blocks the timing-dependent plasticity mechanism in brain slices, the birds lost the ability to alter their song.

Mehaffey credits Doupe's thorough knowledge of songbird behavior and neurology with the success of the experiments, which depended on using electrical stimulation patterns that mimicked the naturalistic patterns of activity observed in the bird brain during song.

"She deeply understood this system and encouraged her students and post-docs to pursue every imaginable method to examine what she thought was an important question," Mehaffey said. "She was fearless in that regard."

Mehaffey and others in the Doupe lab are now working to learn how specific changes to the song are represented at the synaptic level and how a bird integrates these changes into its standard song. Understanding these questions has the potential to teach researchers how the basal ganglia and cortex interact in humans to produce fine motor learning, and how it malfunctions in disease. First-generation drugs for basal ganglia disorders have mainly involved shutting the whole thing down, Mehaffey said.

"When it's malfunctioning, you're better off without it, and that goes for birds and humans," he said. "But it would be nice to get to a point where we understand the system enough to start being able to actually go in and fix what's broken."

Adapted by MNT from original media release

http://www.medicalnewstoday.com/releases/297696.php?tw