Category Archives: Neuroscience

Neuroscience (and a Tiny Dose of Emotional Intelligence) Reveals the Simple Trick to Break Nearly Any Bad Habit – Inc.

Nice piece of grilled salmon. Brown rice. Salad with no dressing. I feltfull: Not stuffed, but satisfied. Better yet,I felt good about having eaten a healthy meal.Then the ice cream called me.

Think you make a lot of decisions? You do, but not as many as you think.Research shows that approximately 40 percent of the things we do on a daily basis aren't decision-based. They're habits.

And someare bad habits.

Which doesn't, at first glance, make sense."We find patterns of behavior that allow us to reach goals," says Dr. Wendy Wood, the author of Good Habits, Bad Habits."We repeat what works, and when actions are repeated in a stable context, we form associations between cues and response."

So why do we form habits that don't help us reach our goals? My goal is to maintain a healthy weight, and eating ice cream is a far fromsupportivepattern of behavior.

Because neuroscience -- theway our brains are made -- oftenworks against us. (H/t to Eric Barker for the underlying science.)

Say I ask myself, "Should I have some ice cream?" My prefrontal cortex -- thebrain region responsible forplanning,decision making,and supporting goal-oriented behaviors-- would answer, "Nope. Your goal is to eat healthy."

Except my orbitofrontal cortex -- the brain region responsible for emotion and reward in decision-making -- would answer, "Dude, you absolutely should! Ice cream is awesome. You love it. It makes you happy. Besides, you can always burn the calories off by working out a little extra tomorrow..."

Because while my prefrontal cortexis alogical and rational kind of guy, he's fairly quiet and subdued. My orbitofrontal cortex? He's a yeller. He's insistent. He loves to get his way.

And he loves to create bad habits.

Or, as Dr. Wood explains inneuroscientificterms, "When our intentional mind is engaged, we act in ways that meet an outcome we desire -- and typically we're aware of our intentions. However, when the habitual mind is engaged, our habits function largely outside of awareness. We can't easily articulate how we do our habits or why we do them...our minds don't always integrate in the best way possible."

In short, give my orbitofrontal cortexa chance and I'll quickly establish some bad habits. I'll do things reflexively, almostwithout thinking.

If I do manage to think, "Wait, should I really have ice cream...?" that little voice in my head getsdrowned out by my orbitofrontal cortex and the force of habit.

And yep, I'm screwed. Now my goal isn't to achieve something positive by repeatingwhat works. My goal is just to satisfy my habit of eating ice cream. So I do. Without really thinking.

Because if I thought about it, I wouldn't be likely to do it.

As Dr. Wood says, "Habits allow us to focus on other things. Willpower is a limited resource, and when it runs out, you fall back on habits." (If you're like me, you can almost feel a switch flipping in your mind that instantly shuts off any rational thoughts.)

So how do you break that cycle?

The answer is simple, yet difficult: You have to force yourself to think: Not before, but during.

Not, in my case,not before I eatthe ice cream -- because that requires willpower I clearly don't have -- but while I'm eating the ice cream.

The key is to reflectupon the actual benefits derivedfroma habit. For me? Ice cream tastes good. Ice cream... well, that's pretty much the list.It don't feel healthier. I don't feel better when I'm finished. In fact, I feel worse;maybe not physically, but definitelyemotionally.

One upside,lotsof downsides.

And then repeat the process, because one period of reflection and introspection won't be enough. I'll probably have to do it several times before it sinks in -- before my orbitofrontal cortex adopts the rewards and emotions involved in not feeling badabout eating ice cream andnot feeling like I'm sabotaging my health and fitness goals.

Then those two voices will speak in unison. My prefrontal cortexwill share all the long-term benefits ofeating healthy. My orbitofrontal cortex will chime in withreasons why skipping theice cream willmakeme feel better in the moment. In emotionalintelligence terms, myemotions will work for me, not against me.

And that's how the habit gets broken.

Try it. Say, like my Inc. colleague Justin Bariso, you want to stop watching YouTube videos when you know you should be working. The next time the urge strikes, don't fight it. Watch a video.

But don't do it mindlessly: Think about what you're watching. Is it entertaining? Do you gain any value from it? Is it more fun -- or more rewarding or fulfilling or satisfying --than doing something else?

What do you really get out of it?

Do that enough times, reflect on the actual feelings and benefits that result from a habit, and in time you'll start to make a different choice.

Because then yourintentional and habitual minds won't have to work againsteach other.

They'll be able to work together.

The opinions expressed here by Inc.com columnists are their own, not those of Inc.com.

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Neuroscience (and a Tiny Dose of Emotional Intelligence) Reveals the Simple Trick to Break Nearly Any Bad Habit - Inc.

Norton Healthcare to open comprehensive neuroscience facility – Norton Healthcare

On June 17, Norton Healthcare will open a comprehensive neuroscience facility unlike any other in the region. This new facility will benefit patients and the community by providing a comprehensive, multidisciplinary neurosciences program with leading-edge technologies and enhanced research and outreach efforts.

The Norton Neuroscience Institute space, located in Norton Medical Plaza III on the Norton Brownsboro Hospital campus, will support patients with many types of neurological conditions, including brain, spinal and nervous system tumors; stroke; epilepsy; migraine and headache; dementia; and memory care. It also will be home to Norton Neuroscience Institutes Cressman Parkinsons & Movement Disorders Center and Cressman Neurological Rehabilitation, as well as a pain management clinic.

The new space encompasses more than 48,000 square feet of clinical, diagnostic, procedural and rehabilitation space. It contains advanced equipment to allow patients to undergo complex neurological testing and procedures at the same site as their routine office visits. Norton Healthcare invested $15 million into the project.

Neuroscience treatment is rapidly evolving, and were committed to bringing the best care to patients throughout this community, said Russell F. Cox, president and CEO, Norton Healthcare. With this location, patients will be able to receive compassionate, specialized care with the newest technology and equipment, all in one convenient location. This space is designed not only to address patients needs but also to aid in the comfort and ease of their care and recovery.

Many neurological conditions require treatment by multiple providers. Having a centralized location will allow the team to more easily collaborate to develop individualized courses of treatment. Located next to Norton Brownsboro Hospitals Comprehensive Stroke Center and Level 4 epilepsy center, the space also will improve access to follow-up care after patients leave the hospital.

Having dedicated space for comprehensive neurological care and rehabilitation will make it much easier for us to convene in person and develop customized treatments for each patient, said David A. Sun, M.D., Ph.D., neurosurgeon and executive medical director, Norton Neuroscience Institute. We believe this level of collaboration sets us apart from other neuroscience centers.

The new Cressman Neurological Rehabilitation space is equipped with the latest rehab technology, including a virtual reality balance assessment system, a driving simulator, robotic-assisted therapy and more, which will help patients recover and develop skills to live independently. It was made possible thanks to a $616,000 grant from the Norton Healthcare Foundation.

More than a decade ago, Norton Healthcare invested $100 million and created a vision to build one of the best neuroscience programs in the country, and this facility will help us realize that goal, said Lynnie Meyer, Ed.D., R.N., CFRE, senior vice president and chief development officer, Norton Healthcare. The Norton Healthcare Foundation has provided millions of dollars in funding to Norton Neuroscience Institute for Cressman Parkinsons & Movement Disorders Center, memory care, and other vital programs. We look forward to continuing to support their impactful work for years to come.

Classes currently offered through the Norton Neuroscience Institute Resource Center, such as tai chi, yoga, Lego therapy and patient support groups, will be offered at the new facility. These programs have been held virtually during the pandemic, but the goal is to go back to in-person classes in the near future.

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WVU Rockefeller Neuroscience Institute first in region, among first in US to offer latest deep brain stimulation technology for patients with…

WVU Rockefeller Neuroscience Institute first in region, among first in US to offer latest deep brain stimulation technology for patients with Parkinson's  WVU Medicine

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WVU Rockefeller Neuroscience Institute first in region, among first in US to offer latest deep brain stimulation technology for patients with...

Global Neuroscience Industry (2020 to 2027) – Key Market Trends and Drivers – ResearchAndMarkets.com – Business Wire

DUBLIN--(BUSINESS WIRE)--The "Neuroscience - Global Market Trajectory & Analytics" report has been added to ResearchAndMarkets.com's offering.

Amid the COVID-19 crisis, the global market for Neuroscience estimated at US$30.3 Billion in the year 2020, is projected to reach a revised size of US$37 Billion by 2027, growing at a CAGR of 2.9% over the analysis period 2020-2027.

Whole Brain Imaging, one of the segments analyzed in the report, is projected to record a 2.6% CAGR and reach US$7.9 Billion by the end of the analysis period. After an early analysis of the business implications of the pandemic and its induced economic crisis, growth in the Neuro-Microscopy segment is readjusted to a revised 2% CAGR for the next 7-year period.

The U.S. Market is Estimated at $8.9 Billion, While China is Forecast to Grow at 2.8% CAGR

The Neuroscience market in the U.S. is estimated at US$8.9 Billion in the year 2020. China, the world's second largest economy, is forecast to reach a projected market size of US$6.6 Billion by the year 2027 trailing a CAGR of 2.8% over the analysis period 2020 to 2027. Among the other noteworthy geographic markets are Japan and Canada, each forecast to grow at 2.6% and 2.5% respectively over the 2020-2027 period. Within Europe, Germany is forecast to grow at approximately 3% CAGR.

Electrophysiology Segment to Record 1.8% CAGR

In the global Electrophysiology segment, USA, Canada, Japan, China and Europe will drive the 1.9% CAGR estimated for this segment. These regional markets accounting for a combined market size of US$3.2 Billion in the year 2020 will reach a projected size of US$3.7 Billion by the close of the analysis period. China will remain among the fastest growing in this cluster of regional markets. Led by countries such as Australia, India, and South Korea, the market in Asia-Pacific is forecast to reach US$4.1 Billion by the year 2027.

Select Competitors (Total 41 Featured):

Key Topics Covered:

I. METHODOLOGY

II. EXECUTIVE SUMMARY

1. MARKET OVERVIEW

2. FOCUS ON SELECT PLAYERS

3. MARKET TRENDS & DRIVERS

4. GLOBAL MARKET PERSPECTIVE

III. MARKET ANALYSIS

IV. COMPETITION

For more information about this report visit https://www.researchandmarkets.com/r/i9nznw

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Global Neuroscience Industry (2020 to 2027) - Key Market Trends and Drivers - ResearchAndMarkets.com - Business Wire

The Neuroscience and the Treatment of Tinnitus : The Hearing Journal – LWW Journals – LWW Journals

Tinnitus, or ringing in the ears, is a common audiological complaint that is extremely heterogeneous in presentation, etiology, and severity.1 Tinnitus affects approximately 50 million Americans,2 with a similar worldwide prevalence.3 It is the number one service-related disability among U.S. veterans, affecting more than 2.17 million military members.4 There is also an increased prevalence of tinnitus in elderly populations, with estimates as high as 20% in adults over the age of 50.5 Tinnitus has many societal and economic impacts, with some studies estimating the annual tinnitus-related health care cost to be between $700 and $2,000 (USD) per individual.6,7

Shutterstock/Axel_Kock, tinnitus, neuroscience, hearing loss.

In addition to its high prevalence, the heterogeneity of tinnitus has complicated both research and clinical management of the disorder.1 Many documented causes of tinnitus include conductive and sensorineural hearing loss, ototoxicity, head and neck injury, and others.8 Tinnitus severity exists on a wide spectrum ranging from mildly bothersome to severely debilitating. The percept itself is also incredibly variable as some patients report a buzzing, whooshing, pure tone, or other indistinct sounds. Yet it remains unclear whether common or different mechanisms underlie tinnitus with different causes and clinical presentations.1 Importantly, there is neither a cure nor FDA-approved drugs for tinnitus. Many current clinical strategies are focused on alleviating the negative emotional effects of tinnitus without addressing the biological processes that underlie the phantom percept. Our review describes the current basic and clinical research of the physiological correlates of tinnitus and mechanism-driven drug development efforts.1

Tinnitus is the persistent, involuntary, subjective phantom percept of internally generated, indistinct, nonverbal noises and tones. In most cases, tinnitus is initiated by acquired hearing loss and maintained only when this loss is coupled with distinct neuronal changes in auditory and extra-auditory brain networks.1 The exact geometry of the electrical patterns of activity that are necessary and sufficient for the generation and maintenance of tinnitus lies within these networks, but the precise patterns and mechanisms remain unclear.1

In the last 30 years, tinnitus has gained more research attention. Recent progress in tinnitus research can be largely attributed to the development of tinnitus behavioral models in rodents beginning in the 1980s. Animal models are either operant or reflexive; both types are predicated on the idea that tinnitus alters the perception of silence. Operant models are based on the training of animals to behave differently in silence vs. noise. Reflexive models are based on differences in innate reflexes in response to acoustic stimulation or silence. While both models have significantly advanced tinnitus research, we propose that operant tinnitus animal models can assess the cognitive aspects of tinnitus and thus are more suitable for determining tinnitus mechanisms.

Utilizing tinnitus animal models, one of the earliest findings in tinnitus animal research is tinnitus-related neuronal hyperactivity in the dorsal cochlear nucleus (DCN),9,10 an auditory brainstem nucleus. A shift in the voltage dependence of KCNQ potassium channels was found to underlie the tinnitus-related hyperactivity and tinnitus vulnerability,11 while compensatory plasticity of HCN cation-specific channels may underlie resiliency to tinnitus after noise exposure.12 In addition to intrinsic neuronal excitability in the DCN, reduced GABAergic10 and glycinergic inhibitory transmission,13 as well as altered spike-timing plasticity between auditory and somatosensory inputs, contribute to tinnitus-related hyperexcitability.14 Tinnitus plasticity mechanisms have also been studied in other auditory nuclei. There have been somewhat conflicting findings in the inferior colliculus (IC). Namely, IC studies show increases, decreases, or no change in neuronal activity in the IC of tinnitus mice.15-20 Abnormal bursting and hyperactivity have been observed in the auditory thalamus.21 This aberrant thalamic firing has been linked to tinnitus22 and is hypothesized to play a role in the generation of pathological brain rhythms.23 Four main tinnitus correlates have been proposed in the auditory cortex: increased spontaneous firing, increased neural synchrony, increased gain, and tonotopic map reorganization. In addition to auditory areas, current research supports the involvement of non-auditory areas such as the parahippocampus and frontostriatal networks. Parahippocampal networks might play a role in the maintenance of tinnitus by encoding the memory of the tinnitus percept and subsequently reinforcing involuntary auditory memory and perception, while the pathological function of frontostriatal networks enhances tinnitus percepts by failing to suppress unwanted or insignificant percepts (gating). Overall, auditory, emotional, mnemonic, and attention networks are involved in the generation, maintenance, and severity of tinnitus.1

There are currently no FDA-approved therapeutics for tinnitus. The most commonly used therapies include sound-based therapies, such as hearing amplification and masking, and counseling or cognitive behavior therapy (CBT). These approaches are designed to decrease the awareness of the percept or manage the emotional effects of tinnitus but do not target the underlying pathophysiological mechanisms. Recently, significant progress has been made toward the development of device-based therapies such as bimodal (auditory and trigeminal or vagus nerve) stimulation, transcranial magnetic stimulation, and deep brain stimulation. These approaches are aimed to reverse pathogenic plasticity or promote corrective plasticity (rehabilitation) in the brain.

We place a special emphasis on mechanism-driven drug development informed by basic research findings.1 Several compounds are under clinical or preclinical investigation for the treatment of tinnitus, including KCNQ potassium channel openers that aim to reduce hyperexcitability in the auditory brainstem, a Group II mGluR agonist to reduce hyperexcitability in the inferior colliculus, NMDAR channel antagonists to reduce excitotoxicity in the cochlea after noise exposure, a glutathione peroxidase (GPx) inhibitor, and a T-type calcium channel blocker to reduce inflammation after noise exposure and in subsequent tinnitus.

A crucial missing piece in tinnitus research is a mechanism-driven classification system that objectively measures tinnitus and accounts for the observed heterogeneity. Perhaps the biggest of these challenges is the lack of an objective tinnitus measurement.24,25 Current tinnitus diagnostic criteria rely on standard audiometry and self-report measures that subjectively assess how bothersome tinnitus is to the patient. The current classification of tinnitus patients also represents a significant challenge. The lack of effective patient stratification likely contributes to negative or conflicting clinical trial results. Given this heterogeneity, a neuroscience-based precision medicine approach will facilitate clinical trials, treatment, and cure. The use of objective neurophysiological measures (e.g., EEG, MRI, MEG, ABR) or biomarkers (e.g., blood or DNA sampling) may be more useful and reduce experimental variability. Taken together, the future of tinnitus research and drug development must include objective measures, mechanism-driven treatments, and precision medicine approaches.26

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Clinical neuroscience and long covid – The BMJ – The BMJ

As of the 8 June 2021, there have been over 170 million cases of covid-19 and 3.7 million deaths worldwide. In the UK, over 4.5 million cases have been reported with a total of approximately 127,500 deaths. [1,2] However, it is well recognised that case numbers and deaths from covid-19 globally are probably under reported.

Beyond the acute symptoms of covid-19, there is the spectre of long covid for many. Estimates suggest that long covid symptoms are found in 13% of patients at 28 days and in 22% 5-12 weeks from the onset of acute infection [3-6]. We simply do not yet know the full scale of the problem.

Long covid may be the result of several possible pathological mechanisms that have not yet been conclusively determined [3,7,8]. A spectrum of risk factors is likely, such as severe acute infection and a lengthy in-patient stay. Demographic factors may play a partolder women and people with a high body mass index seem particularly affected. Neurological and neuropsychiatric symptoms in long covid such as autonomic dysfunction and fatigue are likely to be some of the most challenging problems to understand and treat. Autonomic dysfunction may be found to be a risk factor for symptom persistence, as well as a possible mechanism involved in long covid. [9] To understand the clinical implications of long covid fully, however, more information is required.

So far little evidence is available to guide the management of long covid in clinical practice. Physical and psychological rehabilitation is needed, but only generalised treatment is possible until we understand the patterns and factors causing persistent symptoms. Recommendations from the National Institute for Health and Care Excellence (NICE) for routine blood, cardiac, and respiratory function tests do not include assessment of neuropsychiatric, neurological, and pain symptoms even though these predominate in surveys of patients with long covid. [3] We argue that in-depth assessment from these specialities will provide a more holistic approach to managing patients with long covid. To achieve this, it is necessary for clinical services to be re-aligned to cover shortfalls in funding, staff, and clinical leadership to deliver longterm care to these patients. The economic fallout from the pandemic means that such resources may be scarce for the foreseeable future, but generic treatments based on traditional rehabilitation models may waste valuable time and money unless specific patient vulnerabilities are first identified. To achieve this, evidence should be synthesised in a living format such as a living systematic review (LSR). LSR is defined by the Cochrane community as a systematic review that is continually updated, incorporating relevant new evidence as it becomes available, allowing better use of data from existing electronic health records to enable evidence-based practice.

To date, it is unknown whether covid-19 variants affect the risk of long covid. Different variants seem to affect virulence and acute symptoms, such as anosmia, but it remains unknown whether new variants could trigger unexpected post-infectious symptoms, emulating the possible link between the 1918 influenza pandemic, Middle East respiratory syndrome (MERS), severe acute respiratory syndrome (SARS), and encephalitis lethargica. [11] Furthermore, it remains to be seen whether vaccination in those previously infected affects the risk of long covid.

The fear of influenza-covid co-infection did not materialise until late in 2020. Strict covid-19 restrictions are now being eased in many parts of the world, including the UK. Only time will tell whether this will increase the risk of joint or sequential infections in the future. Covid and influenza vaccinations may reduce the risk of the overall burden of severe acute infection but may not affect prolonged post-infectious symptoms.

Collecting epidemiological data, identifying symptom clusters, and evaluating representative patients on the basis of these could provide insights into long covid. Life-course epidemiological methods may be useful when constructing studies to explore long covid. Intensive clinical research that could be set up rapidly alongside evidence synthesis may lead to a better understanding of the pathophysiology of long covid. Furthermore, such research may benefit patients with pre-existing neurological disorders, such as Parkinsons disease, multiple sclerosis, and chronic fatigue syndrome. [12]

Considerable health resources have been expended on tackling acute covid infections. The successful vaccination roll-out in the UK and internationally promises to reduce acute infection, disease severity, and transmission. The same investment is needed to better understand long covid, and for clinical services to develop long term treatments.

MS Chong, The National Hospital for Neurology and Neurosurgery London Queen Square and Cleveland Street

Ashish Shetty, The National Hospital for Neurology and Neurosurgery London Queen Square and Cleveland Street and University College London NHS Foundation Trust

Shane Delamont, Kings College Hospital London

Mayur Bodani, Kent and Medway NHS and Social Care Partnership Trust and School of Psychology, University of Kent, Canterbury

Peter Phiri, Research & Development Department, Southern Health NHS Foundation Trust and Primary Care, Population Sciences and Medical Education, Faculty of Medicine, University of Southampton

Gayathri Delanerolle, University of Oxford, Oxford

Acknowledgements: This paper is part of the multifaceted EPIC project that is sponsored by Southern Health NHS Foundation Trust and in collaboration with the University of Oxford.

Competing interests: PP has received research grant from Novo Nordisk, and other, educational from Queen Mary University of London, other from John Wiley & Sons, other from Otsuka, outside the submitted work. GD has received funding from the NIHR.All other authors report no conflict of interests for this article.

The views expressed are those of the authors and not necessarily those of the NHS, the National Institute for Health Research, the Department of Health and Social Care or the academic institutions.

References:

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Clinical neuroscience and long covid - The BMJ - The BMJ

Music, Math and Mind: The Physics and Neuroscience of Music (David Sulzer) – Limelight

David Sulzer is the Karl Kruszelnicki music nerds have been looking for. I just wish hed used a catchier title for his book. Because far from being a scientific treatise on the physics and neuroscience of music, Music, Math and Mind is a hugely entertaining, easy-to-understand account of how music works and why it has such an effect on us.

Not only that. Yes, Sulzer is a neuroscientist and currently professor of Psychiatry, Neurology, Pharmacology at the School of the Arts, Columbia University. But hes also an experienced composer, performer and recording artist across several genres, from classical to alt-rock. Just google The Krotopkins or Soldier String Quartet.

Sulzer clearly explains acoustics, musical notation, composition, the physiology of the ear and many other aspects essential to his subject, across time and cultures and using real-world examples. He also offers plenty of exercises and suggestions for listening, again mixing up the genres. After all, there is no room for prejudice or elitism in science. Nor should there be in music.

The maths in each chapter is usually separated out in sidebars with provocative questions like How much does sound weigh? along with fun facts about the length of organ pipes and the worlds most unwanted orchestra. But Sulzers main concern is integration: science and art are two sides of the same coin, and facts are nothing without imagination.

I loved reading about the reconstruction of the c.35,000-year-old Geissneklosterle flute and the Thai Elephant Orchestra. How our solfeggio note names derive from the hymn Ut Queant Laxis by Guido of Arrezzo, inventor of the musical staff for notation. Why equal temperament doesnt work in Indian classical music (try it). And how calcium influx triggers synaptic vesicle fusion. (!)

Frankly, and notwithstanding Sulzers admission that no one needs this book, no musical home or institution should be without Music, Math and Mind.

Music, Math and Mind: The Physics and Neuroscience of MusicBy David SulzerColumbia University Press, PB, 304pp, $46.95ISBN 9780231193795

Available from Booktopia.

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Music, Math and Mind: The Physics and Neuroscience of Music (David Sulzer) - Limelight

Juneteenth and its stories are a part of Joyce Richey’s family history – USC News

Joyce Richey never needed to learn about Juneteenth from stories in books. She first heard about the holiday through her own family history.

Each generation shares stories about her great-grandmother, who was born into slavery in Georgia and remained enslaved until nearly two years after the practice was abolished in 1862. Juneteenth, observed every year on June 19, celebrates the end of slavery.

She said her master did not tell his slaves they were free until the Yankees, as my great-grandmother called them, came and made him tell them, recalled Richey, associate dean for diversity and inclusion at the Keck School of Medicine of USC. She also said that the Yankees told the plantation owner to give each family of freed slaves 10 acres of land and a whole ham.

She doesnt remember receiving any of that. Instead, her father received a hogs head and no land.

Rena Terry Watson, Richeys great-grandmother, was born into slavery in Georgia. (Photo/Courtesy of Joyce Richey)

Richey heard accounts of her great-grandmother, Rena Terry Watson, throughout her childhood. Every couple of years, her extended family would get together for family reunions and talk about their history and how far theyve come since Watsons time.

Juneteenth commemorates the signing of General Order No. 3 by a Union Army general proclaiming freedom from slavery in Texas on June 19, 1865. Slavery had already been outlawed in Texas and the rest of the United States nearly 2 1/2 years earlier when President Abraham Lincoln signed the Emancipation Proclamation, but enforcement of that new law largely fell on Union troops.

Looking back, one of the things that strikes Richey most is her great-grandmothers spirit of forgiveness. Watson was a devout Baptist who forgave the people who owned her and her family.

During an interview with a local newspaper reporter when she passed age 100, Watson said she forgave the white people for the hard times the slaves had after their emancipation.

And while Richey admires her great-grandmothers heart, she questions whether she could have done the same.

I appreciate my great-grandmothers sentiments, her faith and her belief, for mine are similar, she said. However, when you think about the totality of her life experiences, its hard to reconcile. I also know that to move forward, you have to harness those horrific experiences into positivity, making meaningful change.

Its one thing to read it in history books, but its another thing to see it be so proximate. This is our family.

Joyce Richey

I dont want it to come off like Im not forgiving, but its something thats really difficult to digest.

Richey shares this family history with younger relatives and her own children as much as she can.

Its one thing to read it in history books, but its another thing to see it be so proximate, she said. This is our family.

Both of Watsons parents were slaves, and Watsons husband was also born a slave, Richey said. Thats a painful past to unwrap. She thinks about their deprivation and the opportunity missed: None of them were formally educated or given a chance to accumulate wealth while they were enslaved.

The Terry family, shown in a photo from a large reunion gathering in 1988. (Photo/Courtesy of Joyce Richey)

But it also is a testament to how much their descendants have accomplished. The family has grown by the hundreds about 400 have gathered for family reunions and generations of their children have grown up to have fulfilling careers and families.

Richey is an example. She holds a doctorate and is an associate professor of clinical physiology and neuroscience at the Keck School of Medicine. She studies the relationship between obesity, diabetes and hypertension, and the National Institutes of Health and other major funders have supported her research.

There have been great obstacles, but look at the strides that have been made, she said. At the same time, we still have a long way to go.

Watsons life spanned decades that saw triumphs and continued discrimination for Black Americans. She died in 1963, as the U.S. civil rights movement was building momentum. She was reported to have reached age 113.

Most of what Richeys family knows about their great-grandmother and other relatives comes from the research of an unofficial family historian who has traveled throughout the country to track down original documents about the familys life in the United States.

Most of what Richeys family knows about their great-grandmother and other relatives comes from the research of an unofficial family historian. (Photo/Courtesy of Joyce Richey)

Those documents include birth and marriage certificates, as well as records of where their relatives were sold and some of their freedom papers, which certified their non-slave status.

Although this history is sad, Richey believes its important to share it with others. It shows how far people have come in this country and inspires future generations to honor their past.

I think that, in general, we have fallen short by not knowing our stories and not sharing our stories, she said. Commemorations like Juneteenth provide an opportunity to keep those stories alive and teach that history to others. When you hear those stories, I think thats when people have that aha moment, she said.

She is particularly proud of the fact that USC has made Juneteenth an annual celebration. Juneteenth shouldnt be confined to the South, she said: Its impact reverberates throughout the world.

To bring it home to USC and to highlight our faculty and our students in terms of what that means to us, that bodes really well in terms of just understanding one another, bringing those people together, being inclusive and understanding our sense of diversity and why our diverse experiences are so important, she said. It truly speaks to turning our pain into purpose.

Watch Joyce Richey tell her family story during USCs 2020 Juneteenth celebration (music licensed via Accidental Records: Breathe by Matthew Herbert Big Band):

More stories about: History, Race and Ethnicity

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Juneteenth and its stories are a part of Joyce Richey's family history - USC News

The Neural Mechanisms Behind Effective Psychotherapy – Psychiatric Times

The New Neuroscience of Memory

Recent studies have made important discoveries about the neural mechanisms underlying memory. Four are of particular interest. First, memories are not fixed entities; rather, they enter a labile state whenever they are reactivated, and can be modified or updated with new information during a 4 to 6 hour window after reactivation.1 Second, specific episodic (event) memories and semantic (generalizable knowledge) memories are highly inter-related in that they share neural mechanisms, and the latter are a distillation of the former.2 Third, memories that are emotionally charged are remembered better than those that are not.3 And fourth, the activation of emotion appears to be a necessary ingredient of successful outcomes in psychotherapy.4,5

Drawing upon these observations, my colleagues and I hypothesized that there were 3 key ingredients to lasting change in psychotherapy: 1) activating problematic memories and the associated painful affect; 2) concurrently engaging new emotional experiences that change old memories through reconsolidation; 3) reinforcing the strength of new memories and their semantic structures by practicing new ways of behaving and experiencing the world in a variety of contexts. In a 2015 article in a leading neuroscience journal,4 we briefly discussed the application of this model to 4 different psychotherapy modalities, including behavioral, cognitive behavioral (CBT), emotion focused (EFT), and psychodynamic psychotherapies..

Diving Into the Researchand the Clinical Implications

Realizing that there was much more to say about this new way of understanding change in psychotherapy, my colleagues and I published an edited volume, with multiple contributors, that both explains the basic science of memory and outlines a clinical application of our model. The new book, Neuroscience of Enduring Change: Implications for Psychotherapy, expands upon the previous work in 3 sections.6 The basic science section includes chapters on emotion, memory, emotion-memory interactions, the role of language in shaping emotion and memory, and the role of sleep in memory consolidation and reconsolidation. The clinical section includes chapters from leading experts in psychodynamic psychotherapy, CBT, EFT, coherence therapy, and integrative approaches. Each author considers the role of memory reconsolidation in both psychotherapy and in achieving lasting personal change. The final section includes chapters on recurrent maladaptive patterns, a computational neuroscience perspective on the proposed model, and a discussion of a proposed preclinical and clinical research agenda.

Considerable effort was made within and across chapters to promote cross-fertilization between basic science and clinical application. Although it is written for neuroscience-oriented mental health clinicians, all psychotherapists, psychotherapy researchers, and scientists interested in memory, emotion, and their clinical application will find new ideas and practical advice in this book. An independent book review has been published.7

If one takes this model seriously it could influence psychiatric practice in several ways. For example, it is useful to consider how interventions might be adjusted in therapies that have stalled or have failed. Rather than talking about feelings with the goal of promoting insight, it is also important to experience feelings, especially the old painful feelings from which individuals have protected themselves for years, and to juxtapose these feelings with corrective emotional experiences.

Another clinical implication emerges from the observation that consolidation of emotional memories occurs primarily during REM sleep. Because reconsolidation may work in the same way, medications that inhibit REM sleep may be counterproductive to enduring change in psychotherapy. It is therefore important to know that selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitor, tricyclics, and benzodiazepines inhibit REM sleep, whereas trazodone, buproprion, and mirtazapine do not.8,9. The book describes these and other implications and provides a fresh perspective on how psychotherapy practice may be optimized and integrated in psychiatric care.

The Story Behind the Book

My interest in this topic emerged over the course of my 35-year career as an academic psychiatrist. I was initially trained as a clinical psychiatrist and psychodynamic psychotherapist and have continued to practice and supervise residents ever since. I was also fortunate enough to receive research training (resulting in a PhD in experimental psychology) that focused on cognitive neuroscience and functional neuroimaging of emotion. I have found the dialogue between the basic science of psychiatry and its clinical application to be particularly enriching and informative.

In my role as educator, I have become well acquainted with the challenges (eg, significant differences in the theoretical backgrounds, mindset, and clinical interventions required by these different approaches) psychiatry residents face in developing competence in CBT, psychodynamic psychotherapy, and supportive psychotherapy. Because there is a strong interest in finding common factors and common mechanisms across psychotherapy modalities, it occurred to me that a systems neuroscience perspective could provide an integrative mechanistic framework that would highlight commonalities instead of divergences. Moreover, the goal of integrating pharmacotherapy and psychotherapy is likely to be advanced by explaining how each works in brain-based terms. In my efforts to develop a new brain-based model of change in psychotherapy, I have been fortunate to have remarkable collaborators, including Lynn Nadel, PhD, Emeritus Professor of Psychology at the University of Arizona (a pioneer in the newly emerging understanding of memory).

Concluding Thoughts

It is important to emphasize that we have not yet established that change in psychotherapy occurs through memory reconsolidation. One of the conclusions of our book is that a focus of intervention is recurrent maladaptive patterns, which can be understood as an expression of schemas. Schematic memory is a type of semantic memory and, as an area of neuroscientific investigation, it is relatively new. It remains to be demonstrated empirically that schematic memories can be updated with emotional information. If so, it must then be determined whether this applies to psychotherapy. Although research of this type is still underway, it might be argued that it is important to consider the clinical implications of this model if it were true.

Dr Lane is professor of psychiatry, psychology, and neuroscience at the University of Arizona.

References

1. Phelps EA, Hofmann SG. Memory editing from science fiction to clinical practice. Nature. 2019;572(7767):43-50.

2. Ryan L, Hoscheidt S, Nadel L. Perspectives on episodic and semantic memory retrieval. In: Dere A, Easton J, Huston J, Nadel L, eds. Handbook of Episodic Memory. Elsevier; 2008:5-18.

3. Kalbe F, Schwabe L. Beyond arousal: Prediction error related to aversive events promotes episodic memory formation. J Exp Psychol Learn Mem Cogn. 2020;46(2):234-246.

4. Lane RD, Ryan L, Nadel L, Greenberg L. Memory reconsolidation, emotional arousal, and the process of change in psychotherapy: New insights from brain science. Behav Brain Sci. 2015;38:e1.

5. Auszra L, Greenberg LS, Herrmann I. Client emotional productivity-optimal client in-session emotional processing in experiential therapy. Psychother Res. 2013;23(6):732-746.

6. Lane RD, Nadel L, eds. Neuroscience of Enduring Change: Implications for Psychotherapy. Oxford University Press; 2020.

7. Kramer U. Review of Neuroscience of Enduring Change: Implications for Psychotherapy. Am J Psychother. 2021;74:44-45.

8. Doghramji K, Jangro WC. Adverse effects of psychotropic medications on sleep. Psychiatr Clin North Am. 2016;39(3):487-502.

9. Borbly AA, Mattmann P, Loepfe M, Strauch I, Lehmann D. Effect of benzodiazepine hypnotics on all-night sleep EEG spectra. Hum Neurobiol. 1985;4(3):189-194.

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The Neural Mechanisms Behind Effective Psychotherapy - Psychiatric Times

Cala Health and UCSF to develop neuromodulation therapies – Medical Device Network

Cala Health will collaborate with the UCSF team to create non-invasive therapies for critical neurological diseases. Credit: Colin Behrens from Pixabay.

Cala Health has collaborated with the University of California, San Francisco (UCSF), US, to develop tailored peripheral nerve stimulation treatments based on the formers neuromodulation and data science platform technology.

A bioelectronic medicine company, Cala Health combines innovations in neuroscience and technology to create wearable therapies for chronic diseases.

As part of the alliance, the company will collaborate with UCSF Weill Institute of Neuroscience neurology associate professor and neural engineering expert Dr Karunesh Ganguly, as well as others, to develop non-invasive therapies for critical neurological diseases.

Cala Health founder and chief scientific officer Kate Rosenbluth said: Dr Gangulys pioneering research on the precise targeting of electrical stimulation to modulate neural networks provides an exciting path to personalise therapy to each patient.

This partnership takes Cala Health one step closer to reaching our goal to give the millions of patients suffering from debilitating neurological disorders access to non-invasive, efficacious therapies that improve their quality of life.

The technologies licenced from UCSF under this collaboration will aid Cala Health to grow its pipeline of neurology treatments.

Furthermore, the collaboration will boost the companys mechanistic research to create new tailored treatments as well as aiding in incorporating its data science platform to develop software-enabled customised treatment insights for patients in a timely manner.

Ganguly said: In my clinical work, I see the profound impacts of motor impairments from a wide range of neurological conditions such as brain injury and Parkinsons disease, and we are committed to advancing new treatments to enhance motor function.

The UCSF team looks forward to a fruitful partnership with Cala to advance peripheral nerve stimulation as a treatment to improve motor function.

Recently, Cala Health introduced its transcutaneous afferent patterned stimulation therapy, Cala Trio, for treating hand tremors in the movement disorder essential tremor.

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Cala Health and UCSF to develop neuromodulation therapies - Medical Device Network