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Archive for the ‘Neuropathy’ Category

Find Help For Peripheral Neuropathy With Corrective Health – KXAN.com

Sunday, November 21st, 2021

Posted: Nov 15, 2021 / 12:24 PM CST / Updated: Nov 15, 2021 / 12:24 PM CST

According to ClevelandClinic.org, over 100 million people suffer from neuropathy. The condition affects people of all ages but the most vulnerable are older Americans.

Dr. Jarrod Bagley, D.C., founder of Corrective Health, joined Studio 512 Co-Host Rosie Newberry to talk about peripheral neuropathy and how he can help.

Dr. Bagley, how are the nerves affected by neuropathy?

Nerves in the body become damaged and send signals to the brain that translate into pain.The body has a peripheral nervous system that sends signals to the brain and the central nervous system. The damage occurs over time. So, it isnt necessarily something that happens overnight. Therefore, the symptoms, such as a prickly feeling, burning, or tingling in the hands or feet, gradually increase over time.

What things trigger neuropathy?

There are several types of neuropathies.One of the most common forms comes from having diabetes and results from not managing the disease properly.For example, a consistent high level of blood sugar.Also, low vitamin levels, chemotherapy, and even alcoholism can contribute to neuropathy.

Can neuropathy be reversed?

The good news is that in most cases it can be reversed with natural, non-invasive treatments. We can reverse the damage if it has not reached 80% nerve loss. Neuropathy, if not treated by a professional, could lead to being confined to a walker or wheelchair and even amputation. It is important to get evaluated sooner than later. Corrective Health uses no drugs, no injections, and no surgeries. In fact, we have the most advanced non-surgical FDA-cleared treatments available that focus on regenerating nerves and arteries.

I understand you have an offer for our viewers.A $49 Neuropathy Special?

Yes, that includes a personal consultation, exam, and report of findings.

$49 Neuropathy Special for the first 25 callers (retail value of $249.00), which includes a personal consultation with a physician, complete exam, report of findings. Call Corrective Health at 512-263-0040.

That is a great offer for folks suffering from neuropathy.

During the exam, we calculate down to the exact percentage of how much sensory loss you have in your hands and feet. Its critical to calculate the sensory loss early because once you have reached a certain point nothing can be done.

Doctor, if someone is suffering from neuropathy, how soon can they be seen?

We have trained staff ready to address the specific needs and treatments of each patient. Give us a call.There is no reason to live in pain.

If you or someone you know suffers from chronic pain or neuropathy, call 512-263-0040. First 25 callers are eligible for the $49 Neuropathy Special. Visit CorrectiveHealthATX.com to learn more.

This segment is paid for by Corrective Health and is intended as an advertisement. Opinions expressed by the guest(s) on this program are solely those of the guest(s) and are not endorsed by this television station.

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AlgoTherapeutix Completes Phase I for Peripheral Neuropathy Program ATX01, Poised for Phase II Initiation in 2022 – Business Wire

Sunday, November 21st, 2021

PARIS--(BUSINESS WIRE)--France-based biotechnology company AlgoTherapeutix, developer of ATX01, an innovative topical treatment for the pain of peripheral neuropathy, announced today that the ATX01 Phase I trial successfully reached its safety and pharmacokinetics objectives, clearing the way for Phase II development in Chemotherapy-Induced Peripheral Neuropathy (CIPN).

Stphane Thiroloix, Founder & CEO of AlgoTherapeutix, comments : The outcome of this Phase I trial is an important milestone for AlgoTherapeutix. We are delighted that ATX01s innovative approach and formulation did not raise any safety concern, and its PK profile is consistent with our objectives. We are now busy preparing for the pivotal Phase II CIPN study.

Over half of cancer patients treated with chemotherapy - over two million patients in the US and Europe - develop CIPN and experience sensory symptoms and pain in the feet and hands: loss of sensitivity, tingling, burning, cold and intense pain can persist for months to years after treatment. CIPN is a leading cause of modification or interruption of chemotherapy. To this date, no therapeutic approach has offered a satisfactory response for patients and their caregivers, oncologists and pain specialists.

A recent publication in the Journal of Pain describes the exploratory pharmacological impact of high-dose topical amitriptyline in CIPN patients along with the mechanism of action supporting its activity (https://doi.org/10.1016/j.jpain.2020.11.002)

About AlgoTherapeutix : AlgoTherapeutix is a French biotech founded in 2018 to develop innovative solutions for complex pain. In 2020, AlgoTherapeutix raised a 12 M Series A led by Bpifrance and Omnes Capital to move its lead program ATX01 into clinical development. ATX01 is Phase II ready in painful peripheral neuropathy.

More information on AlgoTherapeutix : http://www.algotx.com

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AlgoTherapeutix Completes Phase I for Peripheral Neuropathy Program ATX01, Poised for Phase II Initiation in 2022 - Business Wire

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Diabetic Neuropathy Treatment Industry Growth Forecast Analysis Manufacturers, Regions, Type and Application to 2026 – Northwest Diamond Notes

Sunday, November 21st, 2021

Latest Report on Diabetic Neuropathy Treatment Market size | Industry Segment by Applications (Hospitals , Clinics and Others), by Type (Peripheral Neuropathy , Autonomic Neuropathy , Proximal Neuropathy and Focal Neuropathy), Regional Outlook, Market Demand, Latest Trends, Diabetic Neuropathy Treatment Industry Growth & Revenue by Manufacturers, Company Profiles, Growth Forecasts 2026. Analyzes current market size and upcoming 5 years growth of this industry.

The investors, stakeholders, emerging and established players can leverage the data included in the report to develop impactful growth strategies and improve their position in the current Diabetic Neuropathy Treatment Market landscape. The report provides a thorough assessment of the micro and macro-economic factors that are expected to impact the growth of the Diabetic Neuropathy Treatment Market.

It provides detailed knowledge of upcoming market trends and current conditions in the global market. This report covers the past, present and forecast period for the long-term and collective examination of the Diabetic Neuropathy Treatment market.

Request Sample Copy of this Report @ https://www.nwdiamondnotes.com/request-sample/74964

Pivotal players studied in the Diabetic Neuropathy Treatment Market report:

Propelling Factors & Challenges:

The report provides data associated with the forces influencing the commercialization scale of the global Diabetic Neuropathy Treatment market for and their effect on the revenue graph of this business vertical. The latest trends driving the market along with the challenges this industry is about to experience in the upcoming years are mentioned in the report. The report emphasizes the key driving and restraining forces for this market. The research report sheds light on development factors, business enhancement strategies, statistical growth, financial gain or loss.

By the product type, the market primarily split into:

By the product Applications, the market primarily split into:

Valuable Market Insights Included in the Report

The report addresses the following queries related to the Diabetic Neuropathy Treatment Market

Global Diabetic Neuropathy Treatment Market Pinpoints:

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Diabetes: The ‘tingling’ sensation that can be caused by long-term high blood sugar – Daily Express

Sunday, November 21st, 2021

Diabetes impacts more than 4.9 million people in the UK, with 90 percent of those cases type two, according to diabetes.org. Though diabetes can be managed, if blood sugar levels are left to spike over long periods of time, it can lead to further conditions.

Long-term blood sugar levels can end up causing severe damage to the nerves.

In particular, nerves that receive signals from your hands and feet can be the most affected.

This is known as diabetic neuropathy, an additional condition that currently has no known cure.

Though around 50 percent of people with diabetes may experience nerve pain at some point in their life, it is not always as severe as diabetic neuropathy.

Most often, it is felt as a "tingling sensation" in the hands and feet, according to Healthline.

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"Peripheral neuropathy becomes more likely the longer you have had diabetes.

"Up to one in four people with the condition experience some pain caused by nerve damage."

However, the NHS notes that it can occur for reasons other than diabetes.

The NHS explains: "In some cases, no cause can be identified and this is termed idiopathic neuropathy."

If you have diabetes, your risk for additional side effects are higher if you smoke, drink large amounts of alcohol regularly, or are over the age of 40.

Diabetic neuropathy, though often felt as a tingling feeling, can also feel like numbness.

Fingers, toes, hands and feet are most often affected.

In some cases, burning, sharp or aching pains can be felt in the impacted parts of the body.

Pain may begin mild and grow stronger over time, possibly extending up the arms and legs.

There is no current known cure for the condition.

Instead, the focus of treatment is on maintenance and reducing symptoms worsening.

Options include diet changes, regular exercise and some medications, which can help to reduce blood sugar levels and relieve pain.

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Vaccinations urged against shingles, a viral infection that’s on the rise – Yahoo News

Sunday, November 21st, 2021

Nov. 19There's a life-altering infection out there that's plaguing people 65 and older, but it's not the novel coronavirus.

It's shingles, which is recognizable by a painful rash and blisters that scab and pus. While it looks like a skin rash to the naked eye, it's actually an infection to the nerve tissue buried beneath the skin, initiated by the same virus that causes the scourge of most children chickenpox.

"(It's) not a fun thing," said Neosho resident Karol Meyers, who suffered through a round of shingles recently. "(I'm) hoping I don't ever get it again."

Shingles should never be taken lightly or brushed aside, said Dr. Henry Petry, geriatrician with Freeman Center for Geriatric Medicine.

"Almost all of the people who get it have had chickenpox in their lifetime," he said. "The older you are, the more likely you are to get it. Recent (Centers for Disease Control and Prevention) studies state that 1 out of 3 people probably the age of ... 65 or above are probably going to get it."

When shingles first breaks out, "it is very painful," Petry said. The rash mostly centered on the chest or abdomen, but it can also appear on the head or face a few days following the onset of pain "can blister, and it's usually linear, meaning it goes from the back (of the body or head) to the front."

During that time, people will feel varying degrees of pain, which can flare up anywhere on the body where there are nerves. When shingles "gets back (in the nerves) it's like an infection in that area, and it kind of inactivates it and makes it do funny things it's not supposed to do," he said.

When treated, an episode can last between seven and 10 days. If untreated, "there's the possibility of developing a type of neuropathy," which is damage or dysfunction of one or more nerves that result in sporadic pain, numbness, tingling and muscle weakness for years on end, Petry said.

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"I've had a couple of (patients) who had it, but they didn't get (shingles) around the chest but down their leg, and they developed permanent foot drop from the changes to the sciatic nerve," he said. Petry also said that should the rash appear on the face and blisters form in the eye, it can cause blindness.

These long-term complications of pain and dysfunction "can be very devastating to the quality of life of that person if it's not treated," he said. "The older you are, the more likely you'll have a problem with it."

While it's impossible for two people who previously had chickenpox to pass shingles to one another, it is possible for someone with shingles to pass it to someone who has never previously had chickenpox, he said.

To that end, CDC officials have noticed a slight increase in shingles cases over the past 24 months, most likely due to stresses brought on by COVID-19.

"Stress is a big immune system depressant," Petry said. "Any time that you have a change in your immune system ... that suppresses it, it's down; I don't mean depressed, but you're down" physically. Major stresses, and some back-to-back-to-back stressors lasting for years, "can make your immune system more susceptible to everything, even to the common cold."

There are ways to lessen the risks from shingles. There are three different types of antiviral drugs that work effectively to rid the body of the infection; steroids also help to reduce some of the post-shingles neuropathy symptoms.

But the best and safest way to protect oneself from shingles is to get immunized against it. CDC officials recommend that healthy adults 50 and older get the two-dose vaccine Shingrix. The vaccine, which two years ago replaced a single-dose vaccine, is more than 90% effective at preventing shingles.

Vaccination against shingles "is the one thing that we really, really recommend as you get older ... in order to prevent the spread of it so it can't be a life-altering infection," Petry said.

Kevin McClintock is features editor for The Joplin Globe.

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Broadway Vascular Announces Top-Line Results of 12-Month Retrospective Analysis Evaluating Revascularization of the Lateral Plantar Artery in Diabetic…

Tuesday, October 26th, 2021

Broadway Vascular

Broadway Vascular

SAN ANTONIO, Oct. 22, 2021 (GLOBE NEWSWIRE) -- Broadway Vascular today announced top-line data from a retrospective analysis of Dr. Broadway's revolutionary revascularization technique, involving treating of the lateral plantar artery for treatment of diabetic neuropathy.

Background:

Diabetic neuropathy is a common and debilitating condition for which available treatments are limited. Arterial stenosis or occlusion (blocking of the artery) is the reason behind nerve death and neuropathy. This results in the symptoms of diabetic neuropathy. Dr. Broadway hypothesized that revascularization of the lateral plantar artery will result in regrowth of the nerve fibers, restoring sensation, therefore, treating diabetic neuropathy.

Methods:

In this 12-month retrospective study, individuals with type 2 diabetes and painful diabetic neuropathy were evaluated. The intervention included revascularization of the lateral plantar artery using an atherectomy device with balloon angioplasty. At baseline, all patients complained of neuropathy with burning, tingling or pain. All were confirmed to have neuropathy. Third-party questionnaire data was collected.

Results:

After 12 months, 22 patients were contacted. Twenty-one of the 22 reported improved Quality of Life. Sixteen of the 22 demonstrated significant improvement of symptoms and neuropathy. Five of the 22 demonstrated complete resolution of neuropathy. One patient did not improve. Ages treated ranged from 50-90 years of age. HbA1c treated were 6.3 to 10.6%.

Conclusions:

Improvements were seen in 95% of patients. This retrospective study suggests the potential value of revascularization of the lateral plantar artery for treating diabetic neuropathy.

Diabetic peripheral neuropathy occurs in up to 60% of individuals with type 2 diabetes and is associated with significant morbidity, including gait disturbances, amputations, anxiety, depression and reduced quality of life. The condition manifests with damage to the terminal branches of peripheral nerves and usually first affects small fibers that are responsible for translating pain, light touch and temperature. As neuropathy progresses, large fibers responsible for reflexes and muscle tone are affected, leading to balance and gait problems. Most patients with diabetic peripheral neuropathy present with pain, numbness, or abnormal, spontaneous or induced sensations in the lower extremities1.

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Broadway Vascular is excited to bring to the community this option to help patients improve their quality of life. They understand more studies are needed to validate this treatment. An ongoing study that Broadway Vascular is conducting evaluates nerve regrowth. In this study, patients will have nerve biopsies before and after their treatment.

About Broadway Vascular:

Broadway Vascular, a pioneering and boutique medical practice, offers non-surgical treatments for many endovascular diseases, such as: peripheral arterial disease, enlarged prostate, knee pain, and bleeding from fibroids or hemorrhoids. They also bring extensive experience with renal failure and caring for patients on hemodialysis.

If persons have a history of diabetes, neuropathy, cold feet, hair loss on legs or feet, pain in legs, pain in feet, smoking, high blood pressure, high cholesterol, call Broadway Vascular at 210-465-7015 to see how they can help you or become part of this study.

For more information on Broadway Vascular's office, located at Blanco Road and Interstate 410 in San Antonio, please visit https://broadwayvascular.com.

For More Information Contact:

Helen Ganzehganze@broadwayvascular.com(210) 465-7015

1. Bunner, A., Wells, C., Gonzales, J. et al. A dietary intervention for chronic diabetic neuropathy pain: a randomized controlled pilot study. Nutr & Diabetes 5, e158 (2015). https://doi.org/10.1038/nutd.2015.8

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Applied Therapeutics Reports Biomarker Data from Pilot Trial of AT-007 in SORD Deficiency – Yahoo Finance

Tuesday, October 26th, 2021

Substantial and significant reduction in sorbitol

Company plans to initiate registrational trial by end of 2021

Company to host conference call and webcast today at 8:30 a.m. ET

NEW YORK, Oct. 25, 2021 (GLOBE NEWSWIRE) -- Applied Therapeutics, Inc. (Nasdaq: APLT), a clinical-stage biopharmaceutical company developing a pipeline of novel drug candidates against validated molecular targets in indications of high unmet medical need, today reported biomarker data from a pilot trial of AT-007 in patients with SORD Deficiency.

Sorbitol Dehydrogenase Deficiency (SORD Deficiency) is a rare, progressive, debilitating hereditary neuropathy that affects peripheral nerves and motor neurons. SORD Deficiency affects approximately 3,300 patients in the US and 4,000 patients in Europe. The disease is caused by a lack of the enzyme sorbitol dehydrogenase, responsible for metabolism of sorbitol, which causes sorbitol to accumulate at high levels and become toxic to the body. Sorbitol accumulation results in significant disability, loss of sensory function, and neuromuscular dysfunction.

Patients with SORD Deficiency have 100 times higher sorbitol concentration in their blood compared with unaffected individuals. In a pilot open-label study in 8 SORD Deficiency patients, AT-007 reduced blood sorbitol levels by approximately 66% from baseline through 30 days of treatment. The range of reduction from baseline in patients was 54%-75%. AT-007 was safe and well tolerated in all treated patients.

These results, in addition to preclinical findings, demonstrate that AT-007 has the potential to be the first disease-modifying therapy for SORD Deficiency. The Company plans to initiate a registrational study by the end of 2021. In advance of the registrational study start, patients can now pre-screen to determine whether they have SORD and if they may qualify for the upcoming trial.

Reduction in toxic sorbitol is critically important in patients with SORD Deficiency. This data demonstrates a significant effect on the underlying cause of the disease, said Michael Shy, MD, Professor of Neurology and Director of the Division of Neuromuscular Medicine at the University of Iowa Hospital Carver School of Medicine.

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AT-007 represents an important advancement for patients with SORD Deficiency, and a unique opportunity to meaningfully impact patients lives. We look forward to beginning our registrational trial for this indication in the coming months, said Riccardo Perfetti, MD, PhD, Chief Medical Officer of Applied Therapeutics.

Increased access to screening and early diagnosis can dramatically improve patients lives, and the Company is collaborating with the Charcot Marie Tooth Association and the Hereditary Neuropathy Foundation to improve access to SORD diagnostic testing, and to better understand the perspectives of individuals living with SORD.

Conference Call Information

Applied Therapeutics will host a conference call today, Monday, October 25, 2021, at 8:30 a.m. Eastern Time, to discuss data from a pilot trial of AT-007 in SORD deficiency. To access the conference call, please dial (800) 369-8554 (local) or (409) 937-8917 (international) at least 10 minutes prior to the start time and refer to conference ID 2437605. A live webcast of the call will be accessible on the Events page under the Investor Relations section of the Applied Therapeutics website at http://www.appliedtherapeutics.com. A replay will be available on the Companys website approximately two hours after the event.

About Applied Therapeutics

Applied Therapeutics is a clinical-stage biopharmaceutical company developing a pipeline of novel drug candidates against validated molecular targets in indications of high unmet medical need. The Companys lead drug candidate, AT-007, is a novel central nervous system penetrant Aldose Reductase Inhibitor (ARI) for the treatment of CNS rare metabolic diseases, including Galactosemia, SORD Deficiency and PMM2-CDG. The Company is also developing AT-001, a novel potent ARI, for the treatment of Diabetic Cardiomyopathy, or DbCM, a fatal fibrosis of the heart. The preclinical pipeline also includes AT-003, an ARI designed to cross through the back of the eye when dosed orally, for the treatment of Diabetic retinopathy, as well as novel dual PI3k inhibitors in preclinical development for orphan oncology indications.

To learn more, please visit http://www.appliedtherapeutics.com and follow the company on Twitter @Applied_Tx.

Forward-Looking Statements

This press release contains forward-looking statements that involve substantial risks and uncertainties for purposes of the safe harbor provided by the Private Securities Litigation Reform Act of 1995. Any statements, other than statements of historical fact, included in this press release regarding strategy, future operations, prospects, plans and objectives of management, including words such as may, will, expect, anticipate, plan, intend, and similar expressions (as well as other words or expressions referencing future events, conditions or circumstances) are forward-looking statements. These include, without limitation, statements regarding (i) the Companys plan to initiate a registrational study by the end of 2021, (ii) AT-007 potential to be the first disease-modifying therapy for SORD Deficiency, (iii) the timing of the initiation and completion of our clinical trials, (iv) the likelihood that data from our clinical trials will support future development of our product candidates and (v) the likelihood of obtaining regulatory approval of our product candidates. Forward-looking statements in this release involve substantial risks and uncertainties that could cause actual results to differ materially from those expressed or implied by the forward-looking statements, and we, therefore cannot assure you that our plans, intentions, expectations or strategies will be attained or achieved.

Such risks and uncertainties include, without limitation, (i) our plans to develop and commercialize our product candidates, (ii) the initiation, timing, progress and results of our current and future preclinical studies and clinical trials and our research and development programs, (iii) our ability to take advantage of expedited regulatory pathways for any of our product candidates, (iv) our estimates regarding expenses, future revenue, capital requirements and needs for additional financing, (v) our ability to successfully acquire or license additional product candidates on reasonable terms, (vi) our ability to maintain and establish collaborations or obtain additional funding, (vii) our ability to obtain regulatory approval of our current and future product candidates, (viii) our expectations regarding the potential market size and the rate and degree of market acceptance of such product candidates, (ix) our ability to fund our working capital requirements and expectations regarding the sufficiency of our capital resources, (x) the implementation of our business model and strategic plans for our business and product candidates, (xi) our intellectual property position and the duration of our patent rights, (xii) developments or disputes concerning our intellectual property or other proprietary rights, (xiii) our expectations regarding government and third-party payor coverage and reimbursement, (xiv) our ability to compete in the markets we serve, (xv) the impact of government laws and regulations and liabilities thereunder, (xvi) developments relating to our competitors and our industry, (xvii) the impact of the COVID-19 pandemic on the timing and progress of our ongoing clinical trials and our business in general and (xviii) other factors that may impact our financial results. In light of the significant uncertainties in these forward-looking statements, you should not rely upon forward-looking statements as predictions of future events. Although we believe that we have a reasonable basis for each forward-looking statement contained in this press release, we cannot guarantee that the future results, levels of activity, performance or events and circumstances reflected in the forward-looking statements will be achieved or occur at all. Factors that may cause actual results to differ from those expressed or implied in the forward-looking statements in this press release are discussed in our filings with the U.S. Securities and Exchange Commission, including the Risk Factors contained therein. Except as otherwise required by law, we disclaim any intention or obligation to update or revise any forward-looking statements, which speak only as of the date they were made, whether as a result of new information, future events or circumstances or otherwise.

Contacts

Investors:Maghan Meyers(212) 600-1902 orappliedtherapeutics@argotpartners.com

Media:media@appliedtherapeutics.com

Patients:SORD@appliedtherapeutics.comDottie Caplan, SVP Patient Advocacy and Engagementdcaplan@appliedtherapeutics.com617.417.8114

Applied Therapeutics, Inc.

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Zika virus in UP: Symptoms, treatment and other things to know – Hindustan Times

Tuesday, October 26th, 2021

Uttar Pradesh has reported a case of the Zika virus, which caused havoc in Kerala a few months ago. The Centre has dispatched a multi-disciplinary team to Kanpur in UP where an Indian Air Force personnel tested positive with Zika on October 23.

The local authorities in Kanpur have formed multiple teams and started implementing precautionary action in the affected person's his residential area and the workplace.

According to Kanpur chief medical officer (CMO) Nepal Singh said, as many as 22 samples of people the patient came in contact with have been sent to National Institute of Virology (NIV) in Pune for examination.

What is Zika virus?

The World Health Organization (WHO) defines Zika virus as a mosquito-borne flavivirus that was first identified in Uganda in 1947 in monkeys. It was later identified in humans in 1952 in Uganda and Tanzania, it further said.

The global health body has recorded outbreaks of Zika virus disease in Africa, the Americas, Asia and the Pacific.

Transmission

Zika virus is primarily transmitted by the bite of an infected mosquito from the Aedes genus, mainly Aedes aegypti. These mosquitoes usually bite during the day, peaking during early morning and late afternoon/evening.

This is the same mosquito that transmits dengue, chikungunya and yellow fever.

Zika virus is also transmitted from mother to fetus during pregnancy, through sexual contact, transfusion of blood and blood products, and organ transplantation.

Symptoms

The symptoms of the disease caused by the Zika virus are mild fever, rash, conjunctivitis, muscle and joint pain, malaise or a headache and usually last for 2-7 days.

The symptoms are very similar to other disease. Zika received special attention after the 2015-2016 outbreak in Brazil.

Treatment

No vaccine is yet available for the prevention or treatment of Zika virus infection. Development of a Zika vaccine remains an active area of research, according to WHO.

How to prevent yourself from Zika?

Protection against mosquito bites during the day and early evening is a key measure to prevent Zika virus infection. Special attention should be given to prevention of mosquito bites among pregnant women, women of reproductive age, and young children.

The WHO recommends wearing clothing (preferably light-coloured) that covers as much of the body as possible; using physical barriers such as window screens and closed doors and windows; and applying insect repellent to skin or clothing.

Things to know about Zika virus disease

According to the Centers for Disease Control (CDC) in the United States, Zika is linked to birth defects. Its infection during pregnancy can cause a serious birth defect called microcephaly that is a sign of incomplete brain development.

Zika virus infection is also a trigger of Guillain-Barr syndrome, neuropathy and myelitis, particularly in adults and older children. The infection in pregnancy also results in complications such as fetal loss, stillbirth, and preterm birth.

It also said that returning travellers infected with Zika can spread the virus through mosquito bites and sex. The CDC, in one of its advisories, said that even if the travellers do not feel sick, after returning from an area with risk of Zika, they should take steps to prevent mosquito bites for three weeks so they do not spread Zika to uninfected mosquitoes.

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Zika virus in UP: Symptoms, treatment and other things to know - Hindustan Times

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Heres Why Alger Sold its Nevro Corp. (NVRO) Position – Yahoo Finance

Tuesday, October 26th, 2021

Alger, an investment management firm, published its Alger Small Cap Focus Fund third quarter 2021 investor letter a copy of which can be downloaded here. During the third quarter, the largest portfolio sector weightings were Health Care and Information Technology. The largest sector overweight was Health Care. The portfolio had no exposure to the Financials, Materials, Real Estate, or Utilities sectors. You can take a look at the funds top 5 holdings to have an idea about their best picks for 2021.

Alger, in its Q3 2021 investor letter, mentioned Nevro Corp. (NYSE: NVRO) and discussed its stance on the firm. Nevro Corp. is a Redwood City, California-based medical device company with a $4.2 billion market capitalization. NVRO delivered a -29.93% return since the beginning of the year, while its 12-month returns are down by -25.08%. The stock closed at $121.29 per share on October 22, 2021.

Here is what Alger has to say about Nevro Corp. in its Q3 2021 investor letter:

"Nevro Corp. was among the top detractors from performance. Nevro has developed and commercialized a proprietary high frequency spinal cord stimulation (SCS) system. More broadly, this technology is known as neuromeodulation, which involves treating pain with electrical stimulation. Today, Nevro's technology is primarily used to treat chronic lower back and leg pain. However, the company received FDA approval to use its system for the treatment of chronic pain associated with painful diabetic neuropathy (PDN) in July, which represents a potentially significant market opportunity. We believe Nevros underperformance resulted from the company producing weaker-than-expected results for the three-month period ended June 30 and, more importantly, issuance of guidance for the third quarter that was well below investor expectations. The company also withdrew full-year revenue guidance due to limited visibility regarding COVID-19 related recovery trends and timelines. For the third quarter guidance, Nevro attributed its disappointing outlook to the impact of the pandemic and a slow recovery in procedure volumes as patients appear to be holding off on physician office visits and surgeries. However, investors have also been concerned that Nevro may be losing share to competitors and that SCS market growth has moderated. We have sold the position."

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Based on our calculations, Nevro Corp. (NYSE: NVRO) was not able to clinch a spot in our list of the 30 Most Popular Stocks Among Hedge Funds. NVRO was in 26 hedge fund portfolios at the end of the first half of 2021, compared to 29 funds in the previous quarter. Nevro Corp. (NYSE: NVRO) delivered a -21.28% return in the past 3 months.

Hedge funds reputation as shrewd investors has been tarnished in the last decade as their hedged returns couldnt keep up with the unhedged returns of the market indices. Our research has shown that hedge funds small-cap stock picks managed to beat the market by double digits annually between 1999 and 2016, but the margin of outperformance has been declining in recent years. Nevertheless, we were still able to identify in advance a select group of hedge fund holdings that outperformed the S&P 500 ETFs by 115 percentage points since March 2017 (see the details here). We were also able to identify in advance a select group of hedge fund holdings that underperformed the market by 10 percentage points annually between 2006 and 2017. Interestingly the margin of underperformance of these stocks has been increasing in recent years. Investors who are long the market and short these stocks would have returned more than 27% annually between 2015 and 2017. We have been tracking and sharing the list of these stocks since February 2017 in our quarterly newsletter.

At Insider Monkey, we scour multiple sources to uncover the next great investment idea. For example, lithium mining is one of the fastest-growing industries right now, so we are checking out stock pitches like this emerging lithium stock. We go through lists like the 10 best EV stocks to pick the next Tesla that will deliver a 10x return. Even though we recommend positions in only a tiny fraction of the companies we analyze, we check out as many stocks as we can. We read hedge fund investor letters and listen to stock pitches at hedge fund conferences. You can subscribe to our free daily newsletter on our homepage.

Disclosure: None. This article is originally published at Insider Monkey.

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Ask the GP: Why do my feet feel like they’re on fire? – The Irish News

Tuesday, October 26th, 2021

Q: AFTER a recent one-hour walk I developed a burning feeling and tingling sensation in both feet, which lasted for most of the evening. I walk every other day and have always worn walking boots and thick socks.

GM

A: THE symptoms you've experienced are known medically as paraesthesia - from the Ancient Greek 'para' for abnormal or irregular, and 'aesthesia' for sensation.

As both feet are affected, it suggests you have peripheral neuropathy, a common condition caused by damage to the peripheral nerves which run from the brain and spinal cord to all parts of the body, including the hands and feet.

This damage can disrupt the passage of messages along these nerves, leading to numbness, and burning and tingling sensations, such as you describe.

It can also cause muscle weakness, but this is less common.

More than a quarter of over-65s will develop peripheral neuropathy at some point, with a number of potential causes.

It can occur as the result of spinal problems (for instance, through nerve compression), or as a side-effect of daily medications such as amiodarone (used to treat heart rhythm problems), metronidazole and nitrofurantoin (both prescribed for infections) and phenytoin (an anticonvulsant) - all of which can affect nerve function.

Peripheral neuropathy can also be a complication of shingles, caused by the herpes zoster virus which travels via the nerves.

However, the main cause is diabetes as a result of high blood sugar levels over time damaging the nerves.

So, in the first instance, it is important to ask a few questions: did you experience any weakness in your legs during the walk?

And following the evening when you noticed the pain, were there any residual sensations the next day, or since?

Did you have backache, and/or do you have any seemingly unrelated health problems, such as diabetes, or take daily medications?

If you answer yes, and if your symptoms recur and persist, I would suggest seeing your GP.

Diagnosing peripheral neuropathy can involve a nerve conduction study, where an electrode which produces tiny electrical pulses is placed on the leg, and how well these travel down the nerve is measured.

The treatment for the condition depends on the underlying problem causing it.

Some people with migraine don't experience headaches at all, but do suffer a complete loss of energy

Q: MY granddaughter, now 15, has had a 'weird illness' monthly since she was nine. I can only describe it as a total physical collapse which lasts a few days, with headaches and no energy. It's not premenstrual tension (PMT) and neither the GP nor a psychologist can diagnose it, although blood tests show raised markers.

NA

A: I agree, the regularity of these monthly episodes, taking place 10 days after her period (as you explain in your longer letter) and the total loss of energy and collapse are odd symptoms.

My suggestion is that your granddaughter is suffering from a form of migraine - in her case, the headaches aren't the most significant feature of her attacks. (In fact, some people with migraine don't experience headaches at all.)

In some sufferers, migraine can also cause a complete loss of energy, making them feel exceedingly unwell, with other widespread sensations that are difficult to describe and that sometimes last for three to four days. Patients can also experience nausea or loss of appetite.

As there are no specific diagnostic tests for migraine, it might be worth her trialling one of the triptan drugs (e.g. sumatriptan). These trigger the production of serotonin, a hormone that constricts blood vessels and reduces inflammation.

They are not licensed for children but can be used 'off label' under supervision.

A small dose of sumatriptan, 25mg, under the advice of her GP or paediatrician, could be worth trying, and prove if this suggested diagnosis is correct.

It is a good idea to use a cheap and simple blood pressure monitor at home

IN MY VIEW: We must all know our blood pressure

NOT enough people realise that high blood pressure is a silent killer - no doubt due to the fact that even very high blood pressure causes nothing in the way of symptoms, but by then there's so much damage that full recovery is impossible.

As well as heart attacks, it can lead to the arteries rupturing, causing a stroke - resulting in massive damage or death.

This is why screening for high blood pressure is vital.

One obstacle to accurately monitoring it is that blood pressure is labile - i.e. it jumps about - and some people's jumps up the minute they enter the surgery or set eyes on a doctor, so-called 'white coat' hypertension.

So I applaud the fact that the over-40s can now get free blood pressure checks at chemists. It may well be that the psychologically driven reflex that results in higher pressures when tested at a doctor's surgery will not occur.

Even better, I think, is to buy a simple and cheap blood pressure monitor and to use this at home every few days (or, if your readings are normal, maybe once a month).

That way you'll get the most relaxed - and the most realistic - readings.

Nobody should be seeing regular measurements of blood pressure higher than 140/90.

Daily Mail

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Ask the GP: Why do my feet feel like they're on fire? - The Irish News

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For veterans: VA prepares to tackle backlogged disability claims – The Herald-Times

Tuesday, October 26th, 2021

Steven Miller| Guest columnist

The Department of Veterans Affairs announcedOct.13that it is preparing to hire more than 2,000 new employees to assist in disability claims processing.

According to the VA, more than 204,000 backlogged disability claims are in the Veterans Benefits Administrations' disability claims queue.Many of the claims result from the VA adding three new diseases to the Agent Orange presumptive list. The presumptive list contains the diseases that the VA will presume to have been caused by exposure to Agent Orange.

The three new conditions are hypothyroidism, bladder cancer, and Parkinsonism. With the three new conditions, the VA now recognizes 17diseases caused by Agent Orange exposure. The other diseases areAL amyloidosis, chronic B-Cell leukemias, chloracne, diabetes mellitus type 2, Hodgkins disease,ischemic heart disease, multiple myeloma, non-Hodgkins lymphoma, Parkinson's disease, peripheral neuropathy (either secondary to diabetes or having occurred within one year of leaving Vietnam), porphyria cutanea tarda, prostate cancer, respiratory cancers and soft tissue sarcomas.

If you need assistance filing a VA disability claim or if you have questions about federalstate, or local veterans benefits, please reach out to my office.

Steven Miller is theMonroe County Veteran Service Officer. Callhim at 812-349-2537 or email smiller@co.monroe.in.us.

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Tri-State Neuropathy Centers continues to expand its peripheral neuropathy treatment practice in the tri-state area to continue its mission to help…

Tuesday, August 17th, 2021

Originally known as Neuropathy Treatment Centers of PGH, Tri-State Neuropathy Centers was established in 2013 by Dr. Shawn Richey and served patients only from their Wexford office until 2015 when expansions began. There are now five locations with three of those located in Pennsylvania (Monroeville, Washington, and Wexford), one in Poland, Ohio, and one in Weirton, West Virginia.

Approximately 30 million Americans suffer from peripheral neuropathy and its debilitating symptoms of painful cramping, burning and tingling, numbness in the feet, legs and/or hands, difficulty walking and even interruption of sleep. Tri-State Neuropathys program has had a phenomenal satisfaction rate and has seen thousands of patients suffering with peripheral neuropathy who have tried everything including potentially harmful medications and other painful testing and treatments. This can leave patients still struggling and wandering down the long road of endless disappointment.

With Tri-State Neuropathy Centers innovative treatments, patients now have hope and can have the pain associated with peripheral neuropathy addressed. We have treated over 8,000 patients with a 90% satisfaction rate, and we are confident that we can help improve most anyones life who has been affected by this devastating disease, said Dr. Shawn Richey, CEO, Tri-State Neuropathy Centers.

Tri-State Neuropathy Centers are 100% focused on helping people obtain relief from neuropathy, said Dr. Richey. Our proven treatment protocol is a PAINLESS, NON-INVASIVE AND DRUG-FREE therapy that utilizes advanced technology to reverse the horrible symptoms of peripheral neuropathy. It was once thought that there was no hope for neuropathy sufferers, and now there is.

Paula Connelly sought help in 2020 when her foot became numb after surgery. I was getting very depressed as my foot was numb on the side of the incision and it was affecting my life.I decided to meet with Tri State Neuropathy Centers for a free consultation. I have completed the program I am pain free and 90 percent better. I am 68 and a Grammy of 6 grandchildren.The treatment has helped me walk without a cane and be more active with my active family as my balance has improved tremendously.

Janine Caddys pain was progressing to the point where she couldnt walk. It seems like it became noticeable about 20 years ago. At first my feet would ache from time to time, then my feet would ache so bad that I had to limit my time standing or walking. I could no longer go hiking with my husband or just take a walk. I knew it was just a matter of time before I would need a wheelchair. I heard about Tri-State Neuropathy Centers and went for my free consultation to see if I was a candidate. To date, I see a significant improvement. I can take short walks, cook and I have even been gardening. It feels like a miracle.

Frank Smitts foot condition preventing him from enjoying his usual activities. Ten years ago I hurt my foot and it continued to get worse over the years. It got to the point that my feet were so sore and cold all the time. Outdoor activities are very important to me and I was losing the ability to do them. I felt there was no hope. A friend of mine learned of Tri StateNeuropathy Centers and I made an appointment. The results have been unbelievable. I have no more pain and my feet are no longer cold. My range of motion is so much better, and my balance is back. I am now enjoying all the outdoor activities I use to and am nearly 100% better.

If you are suffering with peripheral neuropathy, you may want to consult Tri-State Neuropathy Centers for a free evaluation. We offer the first initial consultation, examination and first treatment for FREE. We qualify patients to make sure they are candidates for our treatments, and of the over 8,000 patients we have qualified, we have an outstanding success rate, said Dr. Richey.

Patients can call 724-940-9000 to schedule an initial, no-cost consultation to determine if they qualify for the Tri-State Neuropathy Centers treatment program. Additionally, a free confidential online survey is available for patients on the Tri-State Neuropathy website (www.marydancedin.com). Each survey is reviewed by a doctor.

Sponsored content brought to you byTri-State Neuropathy Centers.

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Out of Every Ten Diabetic Patient, At least Seven are Identified with Diabetic Neuropathy – BioSpace

Tuesday, August 17th, 2021

Expanding at 5.9% CAGR, Peripheral Neuropathy to Cement Dominance in Diabetic Neuropathy Treatment Market

The diabetic neuropathy market study by Fact.MR offers compelling insights into key growth drivers and restraints impacting the market through 2031. The survey offers diabetic neuropathy demand outlook and studies opportunities existing in key segments, including type and end user. It also highlights key strategies adopted by market players to increase diabetic neuropathy sales.

Fact.MR A Market Research and Competitive Intelligence Provider: As per the insights by Fact.MR, the global market for diabetic neuropathy is anticipated to rise at a CAGR of 5.6% over the forecast period 2021-2031.

Increasing prevalence of diabetes as a result of changing lifestyles and imbalanced diets is a primary factor, supporting the growth of the diabetic neuropathy market. In 2019, it was found that over 1/10th of the worlds population suffered from diabetes.

Considering this, leading manufacturers are increasingly focusing on incorporating anti-diabetic formulations within their diversified portfolio. For instance, Janssen Global Services LLC, a leading pharmaceutical company offers a wide range of drugs including NUCYNTA, NUCYNTA ER, Duragesic and INVOKANA.

These drugs include tapentadol and canagliflozin, which help in regulating the blood sugar levels. Several other leading pharmaceutical companies are expected to join the bandwagon, while expanding their portfolio. These factors will contribute towards the growth of the diabetic neuropathy market.

Request a report sample to gain comprehensive insights at

https://www.factmr.com/connectus/sample?flag=S&rep_id=4698

Among various types of disorders, peripheral neuropathy segment is gaining traction and exhibiting a higher sales of diabetic neuropathy formulations. As per the Fact.MR, demand outlook for peripheral neuropathy remains optimistic and it is set to expand at a CAGR of 5.9% over the upcoming years.

Besides these, hospitals have emerged as dominant end users owing to the availability of advanced infrastructure and healthcare expertise. Also higher footfall patients will continue supporting growth in demand across hospitals.

According to the study, North America is dominating the market for diabetic neuropathy, accounting for nearly 2/5 of the market revenue across the globe. Owing to factors such as increasing number of patients for getting treatment along with rising investment in research for the development of new drugs, the market in the region is expected to expand considerably over the forecast period 2021-2031.

Increasing emphasis on research and development pursuits along with innovations in drug combinations for fulfilling the dual purpose of providing symptomatic pain relief and preventing the progression of neuropathic processes will bolster future growth prospects, says a Fact.MR analyst.

Key Takeaways from Diabetic Neuropathy Market Survey

Key Drivers

Key Restraints

To learn more about Diabetic Neuropathy Market, you can get in touch with our Analyst at:

https://www.factmr.com/connectus/sample?flag=AE&rep_id=4698

Competitive Landscape

Diabetic neuropathy manufacturers are focusing on receiving certifications from international organizations for their new product launches.

In 2017, Pfizer announced that the U.S. Food and Drug Administration (FDA) approves STEGLATRO(ertugliflozin) tablets, an oral sodium-glucose cotransporter 2 (SGLT2)inhibitor, and the fixed-dose combination STEGLUJAN (ertugliflozin and sitagliptin) tablets

For instance, in 2020, Lupin Pharmaceuticals Inc, received tentative approval from U.S. health regulator to market type 2 diabetes drugs namely Empagliflozin and Linagliptin tablets.

Some of the leading players operating in the diabetic neuropathy market profiled by Fact.MR are:

More Valuable Insights on Diabetic Neuropathy Market

Fact.MR, in its new report, offers an unbiased analysis of the global diabetic neuropathy market, analysing forecast statistics through 2021 and beyond. The survey reveals growth projections on diabetic neuropathy market with detailed segmentation:

Key Questions Covered in the Diabetic Neuropathy Market Report

Explore Fact.MRs Coverage on the Healthcare Domain

Diabetes Diagnostics Market- The demand for diabetes diagnostics is predicted to increase as a result of the COVID-19 outbreak, which has resulted in an increase in hospitalizations. Diabetes test strips are in high demand as a result of studies that show diabetics are at a higher risk of becoming seriously ill if infected with the virus. Government investment for hospitals will help to expand the market overall by making healthcare more accessible in remote areas. The diabetes diagnostics industry will see further growth as the prevalence of obesity rises. Through 2030, the global diabetes diagnostics market will be dominated by players from North America, Asia Pacific, and Europe.

Diabetes Management Software Market- The rising prevalence of type 1 and type 2 diabetes is one of the factors driving the growth of the diabetes management software industry. Diabetes patients are growing as a result of unhealthy lifestyles, poor diets, and rising stress and tensions. As a result, in recent years, the adoption of diabetes management software has increased, resulting in a favourable impact on the diabetes management software market. Another factor driving the growth of the diabetes management software market is technological advancements. One of the most important elements driving the remarkable development in the use of diabetes management software is the increasing number of younger diabetics.

OTC Analgesics Market- Over the last few years, there has been an increase in the use of off-label medications, which are inexpensive and unapproved but effective in treating ailments. Off-label medications such as tricyclic antidepressants, antihistamines, anticonvulsants, selective serotonin reuptake inhibitors, anti-anxiety medicines, and steroids are increasingly being used to treat pain sensations. Because of the widespread availability of over-the-counter analgesics, which are administered with approved medications as maintenance therapy, symptom management linked with pain has become convenient and straightforward. The market for over-the-counter analgesics has shown to have a lot of potential all over the world.

About Fact.MR

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Mahendra SinghUS Sales Office11140 Rockville PikeSuite 400Rockville, MD 20852United StatesTel: +1 (628) 251-1583E: sales@factmr.com

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Out of Every Ten Diabetic Patient, At least Seven are Identified with Diabetic Neuropathy - BioSpace

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CCM can identify nerve damage in patients with long COVID, new study finds – Mobihealth News

Tuesday, August 17th, 2021

New research, released by a team based in Turkey, Qatar, and the United Kingdom, has indicated that a specialised eye exam can be used to identify long COVID.

Published in the British Journal of Ophthalmology, the research found that corneal confocal microscopy (CCM) a non-invasive eye test that conducts real-time imaging of corneal nerve fibres can also potentially be used to confirm suspected cases of long COVID by identifying specific nerve damage.

CCM is also used to identify other conditions, such as diabetic neuropathy, Parkinsons disease, multiple sclerosis, and dementia.

THE LARGER CONTEXT

Penned by researchers from Turkeys Necmettin Erbakan University, Weill Cornell Medicine-Qatar (WCM-Q), and the UKs University of Manchester, the study stated that CCM identifies corneal small nerve fibre loss and increased DCs [dendritic cells] in patients with long COVID, especially those with neurological symptoms.

As a result, CCM could be used to objectively identify patients with long COVID.

The paper added: Long COVID is characterised by a range of potentially debilitating symptoms which develop in at least 10% of people who have recovered from acute SARS-CoV-2 infection.

Symptoms of long COVID include headache, tingling and/or numbness, neuropathic pain, a loss or change in the senses of taste and smell, and so called brain fog.

WHY IT MATTERS

According to a statement by WCM-Q, nerve damage observed in the corneas using CCM can be reliably used as an indicator of nerve damage in other parts of the body.

CCMs value as a diagnostic tool is increased by a number of important factors: the test takes only a few minutes, is completely non-invasive, causes almost no discomfort for patients, utilises existing and widely available ophthalmic equipment, and can be done in the clinic.

ON THE RECORD

The predominance of neurologic symptoms in people with long COVID prompted us to investigate whether CCM could be used to objectively identify nerve damage in patients with the disease, said Rayaz Malik, professor of medicine and assistant dean for clinical investigations at WCM-Q. We are the first group in the world to report a very strong association between nerve damage observed using CCM and long COVID.

Although the majority of people had mild COVID, patients with more severe disease had evidence of greater corneal nerve damage, suggesting that the severity of nerve damage may be related to the severity of disease at presentation.

We believe CCM has the potential to serve as an extremely valuable tool to be used by physicians to help diagnose and assess the evolution of long COVID and to determine the severity in individual cases. The identification of underlying nerve damage also allows us to think about this condition as a neurodegenerative disease, which may be amenable to treatment.

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CCM can identify nerve damage in patients with long COVID, new study finds - Mobihealth News

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Spotlight on ultrasonography in the diagnosis of PND | IJGM – Dove Medical Press

Tuesday, August 17th, 2021

Introduction

Entrapment mononeuropathies are common and contribute to considerable morbidity in the community. The most common entrapment is carpal tunnel syndrome, with an estimated incidence of 197 per 100,000 women,1,2 and much higher rates among employees in certain industries (eg, up to 42% prevalence in poultry workers).3,4 Early diagnosis is essential in entrapment mononeuropathy, to limit nerve injury and associated morbidity. Unfortunately, electrodiagnostic studies (EDX) are frequently non-localising in entrapment neuropathy, and this is the most frequent indication for nerve ultrasound in clinical practice.5 In addition, a significant proportion of EDX are non-diagnostic, between 10% and 25% in CTS for instance, depending on the severity of presentation and EDX protocol used.6,7

Separately, peripheral neuropathy (PN) represents a major cause of morbidity globally,8 and its prevalence is increasing. This has been attributed to the ageing population, an increased prevalence of diabetes and use of neurotoxic drugs such as chemotherapeutics and antiretrovirals.914 The assessment of PN has traditionally relied on neurological assessment, close review of comorbidities and EDX testing. EDX enables neuropathy to be diagnosed, providing information on the pattern of involvement, severity, distinction between axonal and demyelinating pathologies, as well as allowing prognostication and monitoring.15 The clinical and EDX assessment has several limitations however, including a lack of precise anatomical information,15 difficulty diagnosing proximal demyelinating PN,16 and difficulty in distinguishing hereditary from acquired demyelinating PN.17,18 Consequently, there is a need for newer techniques to better diagnose and monitor patients with PN.

Ultrasound using modern, high-frequency probes and image processing provides excellent visualisation of the peripheral nerve, with good spatial resolution and the ability to assess vascularisation with power Doppler. Ultrasound has the further advantage of being able to assess the entire nerve course in real time, whilst being quick, painless, non-invasive, free of radiation and relatively cheap. Ultrasound therefore provides the ideal tool for assessing PN, entrapment mononeuropathy and complements the clinical and EDX assessment. Given the rapid uptake of ultrasound by clinicians, the present review is designed as a practical resource to promote an understanding of the basics of peripheral nerve ultrasound as well as current and emerging applications of ultrasound in the diagnosis of neurological disease.

An ultrasound system uses a transducer to convert electrical current into ultrasound waves via the piezoelectric effect. These waves travel through tissue and are either reflected, refracted, scattered, or absorbed. The amount of resistance an ultrasound beam experiences as it travels through a tissue is referred to as acoustic impedance and is dependent on tissue density. The degree of ultrasound reflection is dependent on the relative differences in tissue densities at a tissue interface, as well as the angle of insonation. Reflected waves are recorded by the transducer and converted into electrical energy which is used to generate our image. The brightness of this image is labelled echointensity (EI) and is proportional to the amount of reflection. This signal is amplified (gain), which can be adjusted. Anisotropy is the loss of echogenicity when an ultrasound beam is not perpendicular to the structure imaged and can be exploited to distinguish peripheral nerves (low anisotropy) from adjacent structures such as tendons (high anisotropy).

The ultrasound image resolution is determined largely by the frequency of the waves, recorded in megahertz (MHz). Higher frequencies allow for greater image resolution, and frequencies greater than 12 MHz are typically utilised for peripheral nerve imaging. In contrast, higher frequencies undergo greater attenuation at increasing depths, and therefore lower frequency ultrasound with better penetration is preferable when imaging deeper structures such as muscle. Consequently, ultrasound imaging is a trade-off between resolution and penetrance, which is achieved in neuromuscular ultrasound by using a transducer with a range of frequencies, for example, 186 MHz. Linear array transducers are typically used in neuromuscular diagnosis, providing a narrower field of view but better resolution at the edges of an image than curvilinear transducers. A smaller footprint probe is sometimes desirable when imaging structures where only limited contact between a probe and the body surface is possible, for instance the hands and feet.

The appearance of peripheral nerves on ultrasound correlates with the microscopic and macroscopic anatomy.19 When viewed longitudinally nerves appear as linear hypoechoic fascicles surrounded by hyperechoic perineurial connective tissue, both enclosed by the bright epineurial connective tissue layer (Figure 1). In cross section, nerves take on a honeycomb appearance of rounded hypoechoic fascicles surrounded by hyperechoic connective tissue (Figure 1). The size and fascicular pattern of healthy nerves can vary depending on location. More proximal nerve segments are typically larger in cross-sectional area (CSA) with fewer or no fascicles, meaning they appear more hypoechoic. This is the result of densely packed fascicles with less connective tissue.20 This process also occurs at fibro-osseous boundaries, for instance the ulnar nerve at the level of the medial epicondyle also appears relatively more hypoechoic even in normal limbs21 (Figure 2D).

Figure 1 Ultrasound appearance of normal nerves. Ulnar nerve imaged in axial/cross-sectional view with honeycomb pattern (A) and longitudinal view with tram track pattern (B).

Figure 2 Normal ulnar nerve and ulnar artery (artery denoted *) in cross section at the wrist (A) in Guyons canal. Ulnar nerve in cross section in the forearm (B), cubital tunnel between two heads of flexor carpi ulnaris (FCU) muscle (C) and between the medial epicondyle (**) and olecranon at the elbow (D).

When differentiating nerves from other structures the following key features can be utilised. Firstly, nerves are surrounded by a hyperechoic rim due to epineurial connective tissue. Secondly, they are more anisotropic than muscle and tendons, meaning tilting the transducer will markedly change the echointensity of these other structures when compared to nerves. Thirdly, unlike blood vessels they are non-compressible, with no pulsatile movement or Doppler flow.

There are several characteristic sonographic features in peripheral nerve injury, including changes in nerve size, echointensity, fascicle dimensions, epineurial boundaries and Doppler signal. Peripheral nerve size increases focally with entrapment and more diffusely in some patients with PN. The cross-sectional area (CSA), measured by tracing inside the hyperechoic epineurium, has a high inter and intraobserver reliability and is highly reproducible.22 The CSA has been widely used to quantify PN, by reference to established normal values for several key peripheral nerves and the brachial plexus.2326 It is important to adjust CSA for normal variability seen across age, sex, height, and BMI.23,24

Echointensity is typically reduced in nerve injury and is usually assessed qualitatively and is usually associated with loss of the normal fascicular architecture described above. Nerve echogenicity can be measured quantitatively using mean gray-scale analysis.21,27,28 Quantitative measures are specific to the individual ultrasound machine used to establish the normative data, limiting their broader application, unless values are normalized using standardized phantoms.

Improvements in ultrasound technology has facilitated measurement of individual nerve fascicles,29 for instance ultra-high frequency ultrasound can identify increased fascicular diameter in immune-mediated PN.30 Fascicular architecture varies from person to person, nerve to nerve and from one anatomical location to another, and there is more work needed to characterise this metric in health and disease.

The Doppler effect is a change in ultrasound frequency reflected from an object, such as a red blood cell, moving toward or away from the transducer. This can be used to demonstrate changes in vascularity of peripheral nerves and surrounding structures. Normal nerve does not have any detectable blood flow. Hence, the presence of Doppler flow is abnormal in peripheral nerves and indicates hypervascularity, which has been described in compressive and inflammatory and some axonal neuropathies.3133

Elastography is a technique used to determine the elasticity of tissue. This is in the form of either strain elastography, in which tissue displacement from extrinsic compression or ambient tissue oscillations is used, or shear wave elastography (SWE), produced by acoustic radiation force impulses generated by the ultrasound probe. Peripheral nerve injury involves the destruction of myelin, which is more compliant, and a proliferation of stiff connective tissue.34 This results in increased stiffness on elastography. There are now several studies supporting the role of both strain and shear wave elastography in diagnosing carpal tunnel syndrome, ulnar neuropathy at the elbow, diabetic PN and even optic neuropathy.35 Further research is ongoing to assess the ability of elastography to diagnose nerve injury in preclinical neuropathy, and to evaluate elastography as a monitoring tool for longitudinal assessment.

Peripheral nerve compression results in nerve enlargement proximal /or distal to the entrapment site on cross-sectional imaging and can appear as an hourglass configuration on longitudinal views (Figure 3).5,36,37 The entrapped nerve may also appear flattened, hypoechoic, immobile and hypervascular.3739 Importantly, up to 42% of mononeuropathy cases studied with ultrasound detect a pathology that alters diagnosis or management, for instance nerve strictures, ganglion cysts or other intraneural or extraneural lesions.40

Figure 3 Normal median nerve and flexor tendons (*) in cross section (A) and longitudinal view (B). Normal median nerve in the forearm (C) superficial to flexor digitorum profundus (FDP) and deep to flexor digitorum superficialis (FDS) muscles. Abnormal median nerve at the wrist (D) with hourglass constriction (white arrows) with swelling proximally at the carpal tunnel entrance (**).

Interestingly, a Sonographic Tinel sign may be present, with clinical symptoms elicited by mechanical pressure from the ultrasound probe at a compression site. Of further interest, chronic nerve compression may result in neurogenic changes to the muscle supplied, such as hyperechogenic and eventually atrophied muscle with fasciculations. The sonographic findings for specific mononeuropathies are summarised below and in Table 1.

Table 1 Diagnostic Sonographic Findings in Compressive Mononeuropathies

The median nerve is optimally studied with the patient seated or lying with the palm facing upward. Imaging can begin at the distal wrist crease, with a cross-sectional view of the median nerve at the entry to the carpal tunnel. The nerve can then be traced proximally as it dives between the flexor digitorum superficialis and profundus in the forearm, and then between the two heads of the pronator teres (another potential site of entrapment).41,42 At the elbow, it runs with the brachial artery, and it can be traced with the artery up to the axilla.

Carpal tunnel syndrome (CTS) results in increased median nerve CSA at the wrist (Figure 3). The ratio of CSA between the wrist and forearm (12 cm proximal to the distal wrist crease), known as wrist to forearm ratio (WFR) will also be increased (Table 1). The median nerve may also be swollen distally at the carpal tunnel outlet, and scanning this region increases the diagnostic sensitivity by 15%20%.43,44 The presence of an immobile, hypoechoic or hypervascular median nerve at the wrist also aids in diagnosis.39 There are several clinical and EDX mimics for CTS, such as benign tumours (neuroma, schwannoma, hamartomas), ganglion cysts, thrombosed vessels or tenosynovitis.45 These are easily diagnosed with ultrasound.45,46 A bifid median nerve can also be identified, which is more prevalent in patients with CTS.47 Ultrasound is useful to assess persistent symptoms post-surgical carpal tunnel release, where it can detect a compressive post-operative scar, a residual anatomical constriction point suggesting incomplete release or an alternative cause for neuropathy.48

In addition, ultrasound can localise a proximal median nerve injury and may help establish a cause, such as entrapment by the ligament of Struthers,49 pronator teres muscle,50 or an accessory palmaris longus muscle,51 as well as vascular pathology52 and iatrogenic injury.53

The ulnar nerve is ideally studied with the elbow flexed at 90 degrees, palm facing upwards and the patient either seated or supine. The Ulnar nerve can be easily located at the elbow in the groove between the olecranon and the medial epicondyle of the humerus (Figure 2C). The nerve can be traced proximally as it runs between the biceps brachii and medial head of triceps brachii en route to join the axillary artery. The nerve can then be traced from the elbow distally as it travels between the two heads of the flexor carpi ulnaris muscle (forming the cubital tunnel) (Figure 2C), before travelling between the flexor digitorum profundus and superficialis as it approaches the ulnar artery (Figure 2B). The ulnar nerve together with the ulnar artery enter the hand superficially via the guyons canal (Figure 2A).

Approximately 76% of ulnar neuropathies are localised to the olecranon groove54 and are typically caused by extrinsic compression or stretch of the nerve resulting in focal demyelination. Focal increase in the ulnar nerve CSA at or above the olecranon is diagnostic.55 The next most common site for injury is at the cubital tunnel due to ulnar nerve entrapment, referred to as cubital tunnel syndrome. Ultrasound demonstrating focal nerve constriction at the entry to the tunnel with proximal swelling is diagnostic. Longitudinal views can aid in localising compression. Both the degree of swelling and hypervascularity are markers of severity56 and axonal loss.57,58 It is important to differentiate cubital tunnel entrapment from compression in the olecranon groove because the former is amenable to surgical release.59 Less common aetiology of ulnar nerve injury can also be identified with ultrasound, including Struthers arcade compression in the upper arm,60 ganglion at the elbow, benign tumours, abscess or anomalous muscles (anconeus epitrochlearis).55 Dynamic ultrasound can also detect a subluxing ulnar nerve, which refers to the migration of the ulnar nerve to the medial epicondyle tip with elbow flexion. Studies assessing the causative role of this abnormality in ulnar neuropathy are conflicting.6163 An elegant study by Omejec et al demonstrated higher rates of ulnar nerve subluxation in patients without a clinical neuropathy, especially those with subclinical ulnar nerve changes on EDX.64

A common dilemma when assessing ulnar neuropathy electrodiagnostically is the inability to localise the dysfunction, and between 14% and 25% of EDX studies are non-localising.65,66 Importantly, the majority of these electrodiagnostically non-localising ulnar neuropathies can be localised with ultrasound.65,66 In addition, ultrasound can readily diagnose ulnar nerve injury at Guyons canal for example due to cycling-related wrist compression,67 intraneural ganglion cyst68 or ulnar artery thrombosis.69

The radial nerve is best imaged with the elbow flexed and the dorsal upper arm directed toward the examiner, so that the posterior course of the nerve above the elbow can be easily traced. The nerve is readily identified in the lateral antecubital fossa, lying above the brachialis and beneath the brachioradialis muscles (Figure 4A). At this location, the nerve starts to divide into the superficial and deep branches. The radial nerve can be traced proximally as it wraps behind the humerus. The radial nerve is then followed up to the spiral groove, between the medial and lateral heads of the triceps brachii muscle (Figure 4B). The nerve can be traced from the antecubital fossa distally as it divides. The superficial branch travels laterally, beneath the brachioradialis and next to the radial artery, before perforating the extensor facia in the distal forearm to reach the anatomical snuff box and provides sensation to the dorsolateral hand and dorsal aspect of digits 13. The deep branch travels medially and dives through the arcade of Frohse (a fibrous arch extending from supinator muscle to lateral epicondyle) as it pierces the supinator muscle (Figure 4C). The nerve then becomes the posterior interosseus nerve travelling over the interosseus membrane and supplying the extensor compartment of the forearm.

Figure 4 Posterior interosseus nerve (PIN) and Superficial radial nerve (SRN) branches of the radial nerve in the cubital fossa (A). Radial nerve branches deep to brachioradialis and superficial to brachialis muscles. Cross section of normal radial nerve in the spiral groove between the triceps muscle and humerus bone (B). Posterior interosseus nerve travelling between the two heads of supinator muscle (*) overlying the proximal radius bone (C). Cross section of abnormal enlarged radial nerve in spiral groove with CSA measuring 35 mm2 (D).

The commonest cause of radial neuropathy is compression at the spiral groove due to extrinsic pressure, known as the Saturday night palsy because it may be associated with sleeping awkwardly when sedated. Ultrasound will show focally increased radial nerve CSA in the spiral groove (Figure 4D). This can be based on absolute increase in CSA or side-to-side comparison (Table 1). Swelling in the radial groove also has prognostic value and predicts a worse clinical outcome at 3 months then radial palsy with normal nerve calibre.70 Another common cause for proximal radial neuropathy is a humeral shaft fracture. Nerve injury secondary to fracture is readily diagnosed with ultrasound.71 The deep motor branch, the posterior interosseus nerve, can be injured at the arcade of Frohse. Causes of this Posterior Interosseus Syndrome may be diagnosed with ultrasound including iatrogenic injury,72 ganglion cysts,73,74 vascular abnormalities,75 tumours76 and entrapment from other structures.77 The superficial radial sensory nerve is susceptible to injury from extrinsic compression, trauma, or mass lesions7880 which may be seen on ultrasound.

The fibular nerve can be identified on ultrasound by first imaging the sciatic nerve in the proximal popliteal fossa (Figure 5A) and tracing it distally as it bifurcates into the fibular (lateral) and tibial (medial) nerves (Figure 5B). The common fibular nerve can then be traced around the head of the fibular bone (Figure 5C). An enlarged and hypoechoic nerve at the fibular head support a diagnosis of compression,24,8183 although care must be taken to not image the nerve obliquely at this location. The deep and superficial fibular nerve branches are more difficult to visualise distally due to their small size and depth, although the deep fibular nerve is readily identified in the anterior ankle. The most common cause for fibular nerve injury at the fibular head is stretch or contusion,84 often associated with significant weight loss, sustained immobility and excessive leg crossing.85,86 However, in one series, as many as 18% of patients presenting with foot drop, have an intraneural ganglion of the fibular nerve identifiable with ultrasound.87 Entrapment of the fibular nerve in the fibular tunnel is a rare cause of fibular neuropathy,88 but this can be seen on ultrasound as a focal stricture of the nerve just prior to the fibular (Figure 5). It is critical to image patients with fibular neuropathy to exclude entrapment and intraneural ganglion, as these patients require surgical decompression whereas non-operative management is indicated for other causes.

Figure 5 Cross-sectional view of the normal sciatic nerve in the distal thigh (A), fibular and tibial nerves in the popliteal fossa (B), fibular nerve at the fibular head (C) and tibial nerve just above the ankle, * denote the ulnar artery (D).

The tibial nerve can also be identified in the popliteal fossa (Figure 5B) before it dives between the heads of the gastrocnemius muscle. The patient is usually examined in the prone position. The tibial is more difficult to identify when running deep in the calf due to the overlying gastrocnemius and soleus muscles but the nerve can be imaged distally as it travels behind the medial epicondyle of the ankle, beneath the flexor reticulum (also known as the tarsal tunnel), in the company of the posterior tibial vessels, tibialis posterior, flexor digitorum longus and flexor hallucis longus tendons. The tibial nerve then branches into the medial and lateral plantar nerves to innervate the sole of the foot.

Ultrasound can identify a cause for distal tibial neuropathy in up to 94% of presentations.89 In one series of 81 ultrasound cases the most prevalent causes were varicose plantar veins, static foot disorders, epineurial ganglion cysts, neuropathies, and iatrogenic injuries. Tarsal tunnel syndrome is a rare compressive mononeuropathy which may be diagnosed on ultrasound by demonstrating an enlarged tibial nerve CSA within the tunnel (Table 1). Ultrasound may also detect a cause in proximal tibial neuropathies, such as bakers cyst90 or soleus arcade/sling.91,92

After significant nerve trauma we may see axonotmesis with interruption of axons but intact connective tissue which acts to guide axonal regrowth. If severe axonotmesis occurs, axonal regrowth occurs proximal to distal at a rate of 1 mm per day. Alternatively, nerve trauma may result in neurotmesis with interruption of both axon and connective tissue. In this circumstance, axonal regeneration is precluded by scar tissue.93 There are several limitations to clinical and EDX evaluation of traumatic peripheral nerve injury. EDX in the acute setting cannot differentiate between a nerve with damaged axons but intact connective tissue and a complete nerve transection.94 This is crucial, however, because complete transection can improve with time-critical surgical intervention. In addition, without imaging one cannot identify other specific anatomical lesions that may require surgery, for instance a painful chronic neuroma,95 or ongoing nerve injury from bone spurs, haematoma, or surgical hardware.96

Importantly, ultrasound can assist in diagnosing and localising a traumatic peripheral nerve injury.95,96 This is visualised by focal swelling and reduced echogenicity, altered fascicular architecture, discontinuity97 or neuroma formation.95 In addition, ultrasound allows the detection of muscle hyperintensity and atrophy secondary to nerve trauma, which often precedes other sonographic and EDX changes.98 In addition, ultrasound can be used to assess whether surgical intervention is required in the setting of nerve discontinuity,96 neuromas99 or bony entrapment.100,101 It is worth noting that ultrasound will not differentiate between severe axonal injury with and without intact epineurium.

Ultrasound also plays a role in surgical planning, by identifying the exact location and length of nerve injury as well as associated structures.20,96,102 Intraoperative high-resolution nerve ultrasound monitoring can also be used103 as it matches closely with intraoperative neurophysiological and neuropathological findings. Following surgical peripheral nerve repair104 ultrasound has a role in identification of partial discontinuity, neuroma formation and compression by overlying scars that may require surgical re-exploration. In a retrospective series of 143 consecutively imaged traumatic peripheral nerve injuries96 ultrasound was 90% sensitive for any nerve injury. The most common abnormalities seen were nerve swelling, followed by neuroma, scar tissue, and discontinuity. Complete nerve transections were infrequent, but readily identified by swollen nerve stumps proximally and distally. The degree of nerve swelling did not correlate with severity of motor dysfunction on EDX.

Thus, ultrasound is an important tool in diagnosing and localising nerve trauma, grading injury, determining the need for surgery and provides useful information in the intra and post-operative setting. In concert with improvements in ultrasound, MRI techniques to visualize the peripheral nervous system such as Diffusion tensor imaging (DTI) have undergone rapid development. DTI with tractography uses water diffusion anisotropy along longitudinal fibre tracts to image nerve pathways.105 DTI has the capability to image nerve injury not identified using EDX or standard imaging techniques.93 In addition, DTI can identify axonal regeneration following traumatic nerve injury with the potential to guide the need for surgical intervention.106

Generalised peripheral neuropathy may be associated with changes on nerve ultrasound. The most prominent changes are identified in demyelinating neuropathies where nerve enlargement is characteristic. Axonal neuropathies are perhaps surprisingly only infrequently associated with reduction of nerve size. The role for ultrasound in diagnosing PN is increasing, and it has the potential to streamline diagnostic algorithms, reduce the need for expensive or invasive investigations and even rationalise costly immunomodulatory and genetic therapies. The following section explores the current ultrasound findings in hereditary, immune mediated and axonal PN.

CIDP is an immune-mediated process typified by multifocal demyelinating nerve pathology in proximal and distal limbs, leading to weakness, sensory loss and reduced deep tendon reflexes. The presentation of CIDP is variable and includes atypical forms such as pure motor or pure sensory CIDP, multifocal acquired demyelinating sensory motor neuropathy (MADSAM) and distal acquired demyelinating sensory (DADS) neuropathy. Abnormal nerve morphology is identified on ultrasound in 6487% of patients.107109Typical sonographic findings are increased nerve CSA in a multifocal pattern, affecting proximal and distal segments and non-entrapment sites110 (Figure 6). Like clinical features, ultrasound findings are similarly variable, with some patients even demonstrating normal nerve size on ultrasound.107

Figure 6 Abnormal median nerve in the forearm in Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), demonstrating multifocal nerve enlargement in longitudinal views (A). Heterogeneous hypo and hyperechoic fascicular enlargement seen of the same nerve in cross section (B) with CSA measuring 68 mm2. Cross sectional view of enlarged median nerve in the forearm with uniform fascicular enlargement seen in Charcot Marie Tooth Type 1A (C) with CSA measuring 62 mm2.

MADSAM is an asymmetric CIDP variant with a more asymmetrical, multifocal pattern of nerve enlargement on ultrasound.111,112 Enlarged hypoechoic fascicles are typically seen in segments with past or present conduction block112,113 and seem to reduce in response to treatment.114

Several distinct ultrasound patterns in CIDP have been identified which correlate with disease duration. Three ultrasound classes were described by Padua et al108 based on CSA and echogenicity. Large hypoechoic nerves (class 1) were associated with the shortest disease duration (04 years) when compared to normal size nerve with hyperechoic changes (class 3) (711 years duration). Large nerves with heterogeneous hypo- and hyperechoic fascicles (class 2) were also heterogenous regards disease duration (0.516 years).

Ultrasound can increase diagnostic accuracy in CIDP, especially when proximal segments and the brachial plexus are imaged.115 This is important because misdiagnosis is common in CIDP, especially in the atypical variants.116 One prospective study assessed 100 suspected chronic immune mediated polyneuropathy referrals with EDX and ultrasound.115 Enlargement in the proximal median nerve or C5 root (referred to as the Short Ultrasound Protocol) was diagnostic with a sensitivity of 84.696.4% and specificity of 44.972.8% depending on the reference standard. Importantly, 25% (11/44) of the those ultimately diagnosed as CIDP/MMN had normal EDX but abnormal ultrasound and were responsive to immunotherapy.

Ultrasound has also been researched as a tool to differentiate between hereditary demyelinating neuropathies, CIDP and other immune mediated PN (Table 2). Various schema has been proposed to quantify these differences. CMT1A is typically associated with the largest nerves, which are homogeneously/diffusely enlarged.107,117 The pattern of enlargement is more variable and to a lesser degree in CIDP. Normal nerve calibre, focal and diffuse enlargement resembling CMT have all been described in CIDP.23,107,109,118 Mild, regional, asymmetrical or heterogenous enlargement all point towards atypical CIDP, MMN, or GBS.23,107 Various imaging protocols and scoring systems have been proposed eg, the homogeneity score and the regional nerve enlargement index.119 The more focal pattern of nerve enlargement seen in inflammatory neuropathies can also be quantified using the intranerve variability (maximum CSA/minimum CSA for a given nerve) and the internerve variability (maximum intranerve variability/minimum intranerve variability for a given patient).120 However, these patterns and scores are predominantly based on relatively small retrospective cohorts, and larger prospective studies are required to define the optimal ultrasound protocols to differentiate these disorders.119

Table 2 Diagnostic Sonographic Findings in Peripheral Neuropathies

Ultrasound provides surrogate markers for disease severity in CIDP, such as hypervascularity, number of nerves involved and cervical nerve root CSA.121,122 Larger nerve CSA has been correlated with slower conduction velocities on EDX testing in many123,124 but not all studies.125 Nerve enlargement has also been associated with clinical weakness and disability.124,125 Additionally, ultrasound provides prognostic information in CIDP, with both decreasing intra-nerve CSA variability and normal or decreasing nerve calibre predicting treatment responsiveness.126

Furthermore, ultrasound has potential as an outcome measure in CIDP. A study of 23 consecutive patients with CIDP followed with serial ultrasound measurements over 3-years, noted CSA increased in 51% of nerve segments, and was associated with increased functional disability and decreased motor nerve amplitudes on EDX.124

GBS is an acute immune mediated generalised polyneuropathy, characterised by ascending sensory disturbance and areflexic weakness, with both demyelinating (acute inflammatory demyelinating polyneuropathy AIDP) and axonal forms (acute motor/sensory axonal neuropathy AMAN/AMSAN). The nadir is typically reached by 6 weeks, and diagnosis is clinical, supported by EDX and cerebrospinal fluid studies.

Proximal nerve and nerve root enlargement has been reported on ultrasound, although the degree and frequency are less then CMT1A and CIDP.23,107 For example, mild enlargement was reported in 8/17 upper limb nerves in one cohort,23 and 5/6 patients in another cohort, although this involved only 9% of the studied nerve segments.127 Importantly, nerve enlargement can be seen as early as day 13 of symptoms,23,128 before EDX changes are apparent.23 The presence of enlarged cervical nerve roots and vagus nerves, together with normal nerve calibre elsewhere can differentiate GBS from CIDP with a positive predictive value > 85%.117 Vagal nerve enlargement on ultrasound has also been correlated with autonomic dysfunction in AIDP.128,129

Some studies have suggested ultrasound can be used to distinguish demyelinating and axonal variants of GBS,130 while other studies have found no difference.131 Mori et al demonstrated enlarged cervical and proximal nerve segments in 6 patients with AIDP, contrasting to enlarged distal nerve segments (forearm, wrist and ankle) in 9 patients with AMAN/AMSAN.130

Miller Fisher Syndrome (MFS) is a rare GBS variant characterised by the triad of ophthalmalgia, ataxia and areflexia, and is often associated with bilateral facial weakness. Hsueh et al132 reported significantly enlarged facial but normal limb nerves in MFS.

Ultrasound has been proposed as an outcome measure for treatment in GBS.129,131 Grimm and colleagues assessed 27 patients with GBS and 31 controls with ultrasound at baseline and 6 months follow up.129 Cervical spinal, medial and vagus nerves were significantly larger in GBS at baseline, but returned to normal at 6 months, except for the vagus nerve which remained enlarged in those patients with significant autonomic dysfunction.

MMN is a rare upper limb predominant demyelinating polyneuropathy characterised by slowly progressive weakness and response to treatment with intravenous immunoglobulin.133135 In practice, MMN can be difficult to distinguish from certain ALS variants.136 Sonographically mild multifocal nerve enlargement, typically in proximal sites and the brachial plexus, is seen in up to 90% MMN patients.137 Ultrasound enlargement can also occur in clinically and electrophysiologically unaffected nerve segments.137

Importantly, nerve and nerve root enlargement on ultrasound can differentiate MMN from ALS. Grimm and colleagues demonstrated that 4 enlarged nerves/nerve roots had a 87.5% sensitivity and 94.1% specificity for distinguishing MMN from ALS in their cohort.138 Others have found that ultrasound is better at distinguishing MMN from ALS then standard EDX assessments.139,140 Ultrasound can occasionally aid in the distinction of MMN from CIDP by the presence of milder, asymmetric nerve enlargement with greater side-to-side intranerve variability, although considerable overlap exists.141

Multiple studies have demonstrated a variable association between ultrasound findings and clinical weakness, disability and EDX abnormalities.139,141,142 Rattay et al demonstrated that the nerve enlargement reduced in parallel with disability after 612 months of treatment in MMN, although baseline nerve enlargement did not correlate with clinical or EDX markers of severity.143 Thus, nerve ultrasound can not only improve diagnosis but also disease monitoring in MMN.

Anti-MAG is an immune mediated demyelinating neuropathy with distally predominant symmetrical sensorimotor impairment and prolonged distal motor latencies on EDX. Despite this the ultrasound abnormalities tend to be proximal144 and there are no reports of distal nerve enlargement. Segmental nerve enlargement has been described in cervical nerve roots, brachial plexus, and proximal nerve segments145 with considerable inter-nerve variability.146 Nerve ultrasound has been used to distinguish anti-MAG neuropathy from similar pathologies. Specifically, nerve size is greater in MAG positive than MAG-negative paraproteinaemic neuropathy.146 Some cohorts found nerve calibre in MAG to be smaller than CIDP.146

POEMS is a rare paraneoplastic multisystem plasma cell disorder causing a mixed axonal and demyelinating polyneuropathy that can mimic CIDP. Pathogenesis is attributed to increased vascular endothelial growth factor leading to neovascularisation and peripheral nerve oedema.147 It is somewhat surprising then, that peripheral nerve ultrasound studies have demonstrated nerve enlargement at entrapment sites only.148 Indeed, the lack of diffuse/multifocal enlargement has been offered as a means of distinguishing POEMS from CIDP.148 However, the published cases describe nerve ultrasound in the subacute setting, after significant secondary axonal degeneration has occurred, and thus the ultrasound findings in early disease remain to be defined.

Brachial neuritis is an idiopathic monophasic inflammatory condition affecting the branches of the brachial plexus. The typical presentation is with severe pain followed by unilateral upper limb weakness. Imaging with ultrasound and other modalities, combined with surgical exploration, have led to greater pathological understanding of this condition. It is now hypothesized that a sequence of nerve enlargement, fascicular adhesion and constriction contributes to ongoing nerve injury.149 Rotational movements of the upper limb are then thought to cause the adhered nerve to tort, with fascicular entwinement and further constriction which has been associated with poor recovery.149 The most common finding on ultrasound, seen in 74% of cases, is unilateral focal nerve enlargement, often affecting the median, radial, anterior, or posterior interosseus nerves.150,151 Other findings include partial nerve constriction, fascicular entwinement or complete nerve constriction with an hourglass morphology, described in up to 50% of cases.152 Early imaging with ultrasound can potentially identify those cases with partial or complete constriction who may benefit from surgical intervention.149,151 Diaphragmatic ultrasound can be used to diagnose phrenic nerve involvement in this condition.

Mononeuritis multiplex is the characteristic pattern of peripheral nerve vasculitis both in isolated nerve and systemic vasculitic disorders. This is reflected on nerve ultrasound by focal, asymmetrically enlarged nerves, in proximal segments without extension to the brachial plexus.153155 Enlargement is described in most EDX affected nerve segments, and prominently in the tibial and fibular nerves.154,156,157 Importantly, nerve enlargement is seen in almost half of all clinically and EDX unaffected nerves.155 Hypervascularity can support a diagnosis of vasculitis PN and is reported in 19% of cases.155 The presence of an axonal neuropathy, with multifocal nerve enlargement proximal to compression sites without plexus involvement is argued to be 94% sensitive and 88% specific for vasculitis.155 Nerve enlargement might reduce with treatment, although this is based on a single case study only.153 Nerve ultrasound has also been suggested as a tool to guide nerve biopsy. Hence, ultrasound can improve diagnosis in PN vasculitis and has the potential to guide biopsy sites and support treatment monitoring.

Hereditary neuropathies are among the most studied conditions in the field of neuromuscular ultrasound. The disorders discussed below are just some of the hereditary conditions that have been studied. There are many others where no data exists.

CMT1A is the most common form of CMT, caused by an autosomal dominant duplication of the peripheral myelin protein 22 gene, resulting in a demyelinating PN. Ultrasound in CMT1A demonstrates diffuse symmetrical nerve CSA increase in 89100% of patients158160 (Figure 6C). This occurs from the brachial plexus and proximal nerve segments to the small sensory nerves such as the sural and auricular nerves.158 Nerve enlargement is detectable from as young as 19 months of age,161 and as such ultrasound is an ideal non-invasive diagnostic aid in young children. Larger CSA has been associated with more severe disease, measured with the CMT neuropathy score.158,162 In addition, a number of studies have demonstrated a correlation between the degree of nerve enlargement and neurophysiological dysfunction,158,162 although this has not been a universal finding.159

CMT1B is another demyelinating form of CMT, due to Myelin Protein Zero mutations. Ultrasound in CMT1B demonstrates nerve enlargement proximally,163,164 but reduced CSA in the lower limbs, helping to distinguish it from CMT1A.164 CMT1X is an X linked mutation of the gap junction associated protein and demonstrates symmetrically enlarged CSA in proximal segments and lower limbs on ultrasound.165 Finally, CMT2 is a heterogenous collection of variably inherited axonal polyneuropathies, with similarly variable findings on ultrasound.100,166

Research into nerve ultrasound as a longitudinal biomarker in CMT has been limited to date. A small study of 15 adults with CMT1A over 5 years failed to demonstrate a change in nerve calibre when assessing the sural and median nerves.167

Although outside the scope of this review, muscle ultrasound in a cohort with CMT has demonstrated reduced thickness and increased echointensity of the first dorsal interossei and tibialis anterior muscles.168 This was more pronounced in CMT1A compared to CMTX1 and CMT2A patients, and correlate with degree of muscle weakness. Consequently, nerve and possibly muscle ultrasound can improve diagnosis and assessments of severity in CMT.

HNPP is caused by an autosomal recessive deletion of the PMP22 gene, leading to multiple painless entrapment mononeuropathies. The classical ultrasound finding in HNPP is multiple areas of nerve enlargement at entrapment sites,169,170 but enlargement at non entrapment sites have also been described.171 Sonographic findings such as CSA do not correlate with neurophysiological parameters, such as the distal motor latency.172

Variant or hereditary transthyretin amyloidosis is an autosomal dominant disorder, where point mutations in the transthyretin gene results in an axonal sensorimotor and autonomic neuropathy. The recent development of disease modifying therapy has prompted great interest in diagnostic and treatment biomarkers. Ultrasound studies in vATTR Amyloidosis have reported increased nerve CSA at entrapment sites, proximal nerve segments and the brachial plexus when compared to healthy controls.100,173 CSA is also greater in symptomatic vATTR then asymptomatic carriers100 and in those with abnormal motor conduction studies.174 While carpal tunnel syndrome is common in vATTR, the median nerve CSA at the wrist is smaller than in idiopathic CTS and is discordant with EDX severity.175 This has been suggested as an early clinical clue for vATTR in patients presenting with CTS.

CANVAS is an adult-onset disorder caused by mutation in the RFC1 gene. A sensory neuronopathy is universally seen in patients with CANVAS,176 and can be detected on ultrasound as a reduction in CSA of the median, ulnar, tibial, and sural nerves.177 A reduced median and ulnar nerve CSA < 5 mm2 in the mid-forearm or mid-humerus demonstrate a sensitivity of 7993%, specificity 100% and area under the curve (AUC) of 0.970.99178 for distinguishing CANVAS from healthy controls.

SCA 2 is an autosomal dominant CAG triplet repeat mutation in the Ataxin 2 gene, resulting in cerebellar ataxia, sensory motor neuropathy, pyramidal and extrapyramidal dysfunction.179 Reduced nerve CSA on ultrasound is seen in the majority (74%) of patients and correlates with the presence of a sensory neuronopathy.177

Friedrich Ataxia is an autosomal dominant GAA triplet repeat disorder affecting the Frataxin gene, leading to cerebellar ataxia, cardiomyopathy and sensory neuropathy/neuronopathy. Interestingly, upper limb nerve CSA is enlarged in Friedrich ataxia, attributed to dysmyelintation and perineurial connective tissue proliferation,180 while lower limb nerve CSA is normal.

The utility of ultrasound in axonal PN is less well characterised. It was hypothesized initially that nerve calibre would be reduced in axonal neuropathies. However, ultrasound has revealed that nerves are typically either normal or slightly enlarged.23,119 The potential application of nerve ultrasound to many forms of axonal neuropathy, eg, toxic, metabolic, inflammatory aetiology remains to be defined by future research.

DPN is characterised sonographically by mild hypoechoic nerve enlargement, notably at compression sites. Several studies have reported enlarged CSA for the median and tibial nerves of Type 1 and Type 2 Diabetics with PN when compared to healthy controls.181184 Nerve enlargement can also predate clinical neuropathy,185 and increases further once DPN develops.186 In addition, the degree of enlargement and vascularity are biomarkers of severity, and correlate with clinical and EDX parameters.182,184,185 Further, in type 2 diabetics nerve ultrasound can demonstrate enlarged fascicles and marked hypoechogenicity when compared to controls, and this to correlates with EDX abnormalities.184,185 Type 2 diabetics with metabolic syndrome also demonstrate larger nerves and more severe neuropathy then diabetics without metabolic syndrome.187 Furthermore, increased tibial nerve stiffness on shear wave elastography is 90% sensitive and 85% specific for diabetes and increases with the development of DPN.188

Chemotherapy-associated PN demonstrates mild, often asymptomatic nerve enlargement at compression sites in 69% of patients and may point to nerve vulnerability to mechanical stress.188 In contrast, Lycan et al studied 20 patients with breast cancer exposed to taxane-based chemotherapy and reported reduced sural nerve calibre on ultrasound.190 Nerve size was further correlated with older age, longer time since exposure and intraepidermal nerve fibre density on skin biopsy.

Leprosy secondary to infection with Mycobacterium leprae is a prevalent cause for PN outside the western world191 and has been well studied with peripheral nerve ultrasound. Leprosy is characterised by both axonal and segmentally demyelinating PN with palpably thickened nerves and skin changes. Leprosy typically manifests with recurrent immune reactions referred to as active leprosy. Ultrasound studies have reported multiple asymmetric nerve enlargement with epineurial thickening.32,192195 Active leprosy is associated with nerve hypervascularisation in 5571% of patients and decreases to 2.75.9% with treatment.193,195 Thus, peripheral nerve ultrasound has potential as both a diagnostic and monitoring tool in Leprosy.193

EDX in children is challenging. EDX testing is potentially painful, with pain more frequently experienced when EMG is performed, when greater than one muscle and proximal muscles are tested.196 It is unsurprising therefore that younger age, especially under 3 years, is associated with inadequate and incomplete EDX in paediatric cohorts.196 Furthermore, EMG relies on active muscle recruitment and patient participation which is limited in the very young.197 Nerve imaging with MRI in children is also challenging due to the need to lie still for prolonged periods which may necessitate sedation. Nerve ultrasound on the other hand is painless, quick, adaptable, cost effective and well tolerated in paediatric patients.198 It seems natural therefore to see a recent growth in paediatric neuromuscular ultrasound research.107,199

Peripheral nerves increase in size as we age, meaning children with enlarged nerves may be incorrectly interpreted as normal if adult references values are applied. Therefore, the accurate interpretation of abnormal nerve CSA is reliant on the ongoing expansion age-specific normative ultrasound data.200,201 Zaidman et al23 examined 40 healthy children aged 217, among a larger cohort of 90 adults and children, and reported a range of normal CSA values. Of interest, an association between height and nerve CSA was seen, and was stronger in children (r =0.9, P < 0.001) than adults (r = 0.5, P < 0.001). Cartwright et al202 recorded peripheral nerve CSA in a further 43 children aged 3 months to 16 years as well 160 adults. Age was the strongest predictor of nerve CSA, although height and BMI were also predictive. Druzhinin et al201 systematically collected ultrasound CSA measurements in an children and young adults, scanning 72 healthy subjects aged 230 years. Their data suggest that nerve CSA is independently associated with age and weight but not height, differing from previous studies by Zaidman23 and Cartwright.201 Zaidman and Cartwright analysed for associations using pooled CSA values from all nerve measurements while Druzhinin analysed each nerve measurement individually, and this may explain their different findings. All three studies found nerve size plateaued at 1214 years leading the authors to conclude that paediatric specific normative values are essential to interpret imaging in subjects below this cut off. The intra and inter-nerve variability was measured in Zaidman and Druzhinins populations and interestingly did not differ significantly with age.23,201 This may be a potential age-independent measure to use where normative data is limited.

Entrapment mononeuropathies are uncommon in children, and when they do occur ultrasound can detect unusual causes such as mucopolysaccharidosis.203,204 Research in adult populations has been used to argue for supplementation or even replacement of standard EDX assessments with neuromuscular ultrasound in certain focal mononeuropathies such as carpal tunnel syndrome.46,205,206 A similar argument could be made for children with mononeuropathies but will require further studies to evaluate.

Polyneuropathies on the other hand are common in children and sonographic nerve changes are detectable in certain hereditary neuropathies such as CMT from a very young age.107,161 Further, nerve CSA in children with CMT1A correlates with disease severity, as well as age, height and weight.161 Furthermore, ultrasound can aid in the distinction between hereditary and acquired inflammatory polyneuropathies in this age group.107,119 Zaidman et al performed nerve ultrasound in 128 adults and children with a range of hereditary and acquired peripheral neuropathies. Thirty-five CMT1 patients age 271 years were examined and 8 out of 9 children with CMT demonstrated diffuse sonographic nerve enlargement.

Ultrasound has also been used to assess neonatal brachial plexopathy, which occurs in up to 3 in 1000 live births.207 The current standard is a 3-month period of observation for spontaneous recovery followed by surgical exploration where recovery is poor.208 In 2015, Somashekar et all compared preoperative US to surgical exploration in the detection of traction neuromas in 33 children.209 Of their cohort, 31 of the 33 surgically identified neuromas were detectable on US. Furthermore, muscle atrophy was identified in 11 children and guided spinal accessory and supra scapular nerve transfers in 8 of those patients.

Another advantage of ultrasound is its potential to limit the amount of EDX testing required to achieve a diagnosis. Rardin et al210 compared retrospective data from 21 children who were assessed by ultrasound prior to EDX with 84 aged-matched control subjects who had EDX assessment alone. Those subjects investigated with ultrasound first required less EDX tests, with fewer nerve stimulations and fewer muscles sampled by EMG. This led the authors to conclude an ultrasound first approach should be considered in paediatric patients to limit EDX testing.

Therefore, ultrasound has a number of distinct advantages in paediatric neuromuscular assessment and its role is likely to grow in this population. Further studies are needed to better define normal nerve size, as well as more detailed structural assessment such as fascicle measurements, echotexture and elastography.

Disorders of the motor neuron include Amyotrophic Lateral Sclerosis (ALS), Spinal Muscular Atrophy (SMA) and Spinal Bulbar Muscular Atrophy (SBMA or Kennedys disease) and Poliomyelitis. Diagnostic delay is a significant issue in these disorders, for instance in ALS the median time to diagnosis is 11.5 months after onset of symptoms.210 In SMA, the emergence of disease modifying therapy has generated the need for accessible, accurate, responsive, and reliable outcome measures. Hence, ultrasound has clear potential to improve the diagnosis and monitoring of motor neuron disease, and there is a growing body of literature supporting its use in ALS and SMA.

ALS is a fatal neurodegenerative disorder affecting the motor neuron, with a median survival of 35 years,212214 characterised by dysfunction of both upper and lower motor neurons (UMN and LMN) as well as cognition.213 Clinical heterogeneity exists, and there is an absence of pathognomonic investigations, leading to significant diagnostic delay.215 To better define the investigations of ALS and to promote recruitment of patients to clinical trials, the El Escorial and revised El Escorial (rEEC) were developed incorporating the presence of upper (UMN) and lower motor neuron (LMN) signs.216218 It was argued that the rEEC, although specific, was lacking in sensitivity, particularly in the early stages of disease, and consequently the Awaji criteria and more recently the Gold Coast criteria were developed.220224 These included the identification of fasciculations on EMG as an LMN sign and have contributed to the increased sensitivity in diagnosing ALS.216,224226 Neuromuscular ultrasound offers greater sensitivity then EMG in the detection of fasciculations especially in bulbar structures and thus has the potential to further improve the diagnostic sensitivity of the criteria.228 Further, muscle ultrasound in ALS can improve diagnosis through the detection of reduced muscle thickness and increased muscle echointensity98,227229 (Figure 7). Furthermore, quantitative measures of muscle echotexture have been used as diagnostic biomarkers and responsive outcome measures in ALS.230,231

Figure 7 Cross-sectional image of a normal tibialis anterior muscle (A) and quadriceps muscles (C) in a healthy individual. Cross-sectional image of abnormal tibialis anterior muscle (B) and vastus intermedius muscle and to a lesser extent rectus femoris muscle (D) in a person with amyotrophic lateral sclerosis. Note in the abnormal muscles there is atrophy with increased brightness or echointensity with a loss of the underlying bone reflection (*).

A reduction in motor nerve and cervical nerve root calibre with a sparing of sensory nerves has been consistently described in ALS232235 and is likely to reflect motor axon loss. This occurs in both clinically affected and unaffected regions.233 Nerve ultrasound can distinguish ALS from mimic disorders such as MMN and peripheral nerve hyperexcitability syndromes.236 Specifically an increased distal:proximal CSA ratio of the median nerve can distinguish ALS and reflects the relative density of motor fibres in the proximal portion of the nerve.236 Additionally, nerve ultrasound is abnormal in preclinical ALS where axonal degeneration is compensated and thus muscle wasting/weakness not yet apparent.233,237 Detecting the submillimetre nerve CSA changes in this preclinical state will likely improve as higher frequency ultrasound probes are developed and in wider use.237,238 One current limitation of nerve ultrasound is its insensitivity as a tool to monitor disease progression.238 Furthermore, nerve ultrasound measurements are not consistently correlated with disease severity on clinical and EDX measures, in part due to the confounding effect of UMN dysfunction.235

Bulbar motor neuron dysfunction, associated with dysphagia, is common in ALS, and can be measured by ultrasound in several ways. Video ultrasonography, a technique to dynamically assess tongue position and morphotexture during attempted swallow, is an early and sensitive measure of dysphagia in ALS.239 Further, ultrasound measures of tongue thickness are reduced in ALS, and this is most marked in those patients with bulbar onset disease and lower BMI.240 Furthermore, tongue thickness decreases with disease progression and may be used to monitor dysphagia and potentially guide timing of nutritional interventions such as parenteral feeding which are associated with improved survival in ALS.241,242 Lastly, minimal change in tongue thickness during swallowing, measured as a reduced thickness ratio is a specific marker of UMN bulbar dysfunction.243 Thus, dynamic tongue ultrasound has potential as a diagnostic and prognostic biomarker of bulbar dysfunction in ALS.

Respiratory dysfunction is universal in ALS as the disease progresses.244 Monitoring respiratory dysfunction, traditionally with spirometry, is essential to guide institution of non-invasive ventilation which can improve survival and quality of life.244246 A major limitation of spirometry in ALS is its poor reliability in the setting of bulbar and facial weakness as well as cognitive impairment. Dynamic diaphragmatic ultrasound thickness, measured as inspiration:expiration thickness or thickening ratio, offers an alternative measure in such patients. Ultrasound diaphragm thickness and thickening ratio are reliable in ALS,247 and correlate with vital capacity, hypercapnia, hypoventilation and motor disability more broadly.247 Thus, diaphragmatic ultrasound represents an important diagnostic biomarker for respiratory dysfunction in ALS,248 although at this stage it remains experimental and is not a substitute for standard measurements.

SMA is an autosomal recessive disorder of spinal lower motor neurons, caused by the mutation in the survival motor neuron (SMN1) gene. This ranges in severity from the severe type 1 SMA with onset before 6 months of age to Type 4 SMA with adult onset. There is considerable interest in biomarkers for diagnosis and disease progression in SMA due to the emergence of disease modifying therapy in the form of antisense oligonucleotides (Nusinersen and Risdiplan) and the gene replacement therapy (onasemnogene abeparvovec-xioi). Nerve ultrasound can distinguish adult onset SMA from mimicking disorders such as CIDP and MMNCB, based on reduced proximal nerve and nerve root CSA in SMA.249

In addition, high-frequency nerve ultrasound may provide prognostic information. This was suggested in a pilot study of 3 SMA patients using ultra high-frequency median nerve imaging.250 A reduced median nerve CSA and fascicle number was seen in the most severely affected subject (SMA I) relative to controls. Further, quantitative muscle ultrasound echo intensity, expressed as a Luminosity ratio, was increased in a cohort of SMA II and III subjects compared to healthy controls.251 Luminosity ratio was higher in more severe disease (SMA II) and correlated with dynamometry measures of strength. This suggests the diagnostic and monitoring potential for muscle ultrasound in SMA. Further research is needed to assess the role of nerve and muscle ultrasound in SMA.

The use of ultrasound to assess peripheral nerves in routine clinical practice is increasing due to its safety, accessibility, and dynamic quality. Current ultrasound technology provides excellent resolution of peripheral nerves and the flexibility of point of care machines allow easy integration into neuromuscular and electrodiagnostic clinics. Ultrasound adds critical structural information to compliment clinical and EDX assessments, contributing to improved diagnosis and pathophysiological understanding of peripheral nerve disorders. While nerve ultrasound is most frequently used to diagnose focal compressive mononeuropathy, its application has grown to include traumatic nerve injury, generalised peripheral neuropathy, motor neuron diseases and a range of other neuromuscular conditions in both adult and paediatric populations. Despite the operator-dependant nature of ultrasound, further development of quantitative measures, standardised protocols and consensus scoring frameworks will allow wider application and lead to improved diagnosis of peripheral nerve disease.

Funding support from the National Health and Medical Research Council of Australia is gratefully acknowledged.

Professor Matthew C Kiernan reports grants from NHMRC, is the Editor-in-Chief of Journal of Neurology, Neurosurgery & Psychiatry, during the conduct of the study. The authors report no conflicts of interest in this work. There are no financial interests or other conflicts of interest to declare.

1. Latinovic R, Gulliford MC, Hughes RA. Incidence of common compressive neuropathies in primary care. J Neurol Neurosurg Psychiatry. 2006;77(2):263265. doi:10.1136/jnnp.2005.066696

2. Hulkkonen S, Lampainen K, Auvinen J, Miettunen J, Karppinen J, Ryhnen J. Incidence and operations of median, ulnar and radial entrapment neuropathies in Finland: a nationwide register study. J Hand Surg Eur Vol. 2020;45(3):226230. doi:10.1177/1753193419886741

3. Musolin K, Ramsey JG, Wassell JT, Hard DL. Prevalence of carpal tunnel syndrome among employees at a poultry processing plant. Appl Ergon. 2014;45(6):13771383. doi:10.1016/j.apergo.2014.03.005

4. Musolin KM, Ramsey JG. Carpal tunnel syndrome prevalence: an evaluation of workers at a raw poultry processing plant. Int J Occup Environ Health. 2017;23(4):282290. doi:10.1080/10773525.2018.1474420

5. Gonzalez NL, Hobson-Webb LD. Neuromuscular ultrasound in clinical practice: a review. Clin Neurophysiol Pract. 2019;4:148163. doi:10.1016/j.cnp.2019.04.006

6. Jablecki CK, Andary MT, Floeter MK, et al. Practice parameter: electrodiagnostic studies in carpal tunnel syndrome. Report of the American Association of Electrodiagnostic Medicine, American Academy of Neurology, and the American Academy of Physical Medicine and Rehabilitation. Neurology. 2002;58(11):15891592. doi:10.1212/wnl.58.11.1589

7. Boonyapisit K, Katirji B, Shapiro BE, Preston DC. Lumbrical and interossei recording in severe carpal tunnel syndrome. Muscle Nerve. 2002;25(1):102105. doi:10.1002/mus.10002

8. MacDonald BK, Cockerell OC, Sander JW, Shorvon SD. The incidence and lifetime prevalence of neurological disorders in a prospective community-based study in the UK. Brain. 2000;123(Pt 4):665676. doi:10.1093/brain/123.4.665

9. Simmons Z, Feldman EL. Update on diabetic neuropathy. Curr Opin Neurol. 2002;15(5):595603. doi:10.1097/00019052-200210000-00010

10. Kandula T, Farrar MA, Cohn RJ, et al. Chemotherapy-induced peripheral neuropathy in long-term survivors of childhood cancer: clinical, neurophysiological, functional, and patient-reported outcomes. JAMA Neurol. 2018;75(8):980988. doi:10.1001/jamaneurol.2018.0963

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Eye scan could determine whether COVID patients will be long haulers – WGNO New Orleans

Tuesday, August 17th, 2021

(StudyFinds.org) Long COVID continues to confound doctors as patients still struggle with debilitating symptoms months after first being infected. A new study now suggests that COVID patients who could be long-haulers could be diagnosed by taking a close look at their eyes. Nerve fiber loss and an increase in key immune cells on the surface of the eye may be a way of identifying the long term impact of the virus, say scientists.

The changes are particularly evident among those with neurological symptoms, such asloss of taste and smell,headache, dizziness, numbness, and neuropathic pain. Doctors at Weill Cornell Medicine-Qatar say long COVID ischaracterized by a range of symptomswhich continue for more than four weeks after the acute phase of the infection has passed, and which arent explained by an alternative diagnosis.

CCM has been used to identify nerve damage and inflammatory changes attributable to diabetic neuropathy,multiple sclerosis, and fibromyalgia..

Forty people who had recovered from confirmed COVID-19 infection between one and six months earlier completed a National Institute of Health and Clinical Excellence (NICE) questionnaire. Data was used to find out if they had long Covid, with a total score ranging from zero to 28. Neurological symptoms were present at four and 12 weeks in 22 out of 40 patients (55 percent) and 13 out of 29 (45 percent), respectively, according to the findings published in theBritish Journal of Ophthalmology.

The participants corneas were then scanned using CCM to look for small nerve fiber damage and the density of dendritic cells. These have a key role in the primaryimmune system responseby capturing and presenting antigens from invading organisms.

The corneal scans were compared with those of 30 healthy people who hadnt been infected by COVID.

Results show that 55 percent of theCOVID patientshad no clinical signs of pneumonia. Twenty-eight percent had clinical signs of pneumonia not requiring oxygen therapy. Ten percent had been admitted to hospital with pneumonia and received oxygen therapy, and 8 percentt with pneumonia had been admitted to the intensive care.

The corneal scans revealed that patients with neurological symptoms for four weeks after they had recovered from acute COVID-19 had greater corneal nerve fiber damage and loss, with higher numbers of dendritic cells, than those who hadnt been infected by the virus. Those without neurological symptoms had comparable numbers of corneal nerve fibers as those who hadnt been infected with COVID, but higher numbers of dendritic cells.

The questionnaire responses indicative oflong COVID symptomscorrelated strongly with corneal nerve fiber loss, says study author Professor Rayaz Malik in astatement.

He notes that it was an observational study, and as such, cant establish cause, and only a small number of participants were involved.

To the best of our knowledge, this is the first study reporting corneal nerve loss and an increase in [dendritic cell] densityin patients who have recoveredfrom COVID-19, especially in subjects with persisting symptoms consistent with long COVID, he adds. We show that patients with long COVID have evidence of small nerve fiber damage which relates to the severity of long COVID and neuropathic as well as musculoskeletal symptoms. Corneal confocal microscopy may have clinical utility as a rapid objective ophthalmic test to evaluate patients with long COVID.

South West News Service writer Stephen Beech contributed to this report.

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Diabetic Neuropathy Treatment Market Trends and Forecast to 2027 Players are Abbott, Roche, Eli Lilly – The Manomet Current

Tuesday, August 17th, 2021

The Diabetic Neuropathy Treatment Market is expected to account for a robust CAGR of 5.6% during the forecast period of 2021-27. The market held a CAGR of xx % in 2021 and xx USD billion in terms of revenue.

Once the immediate and direct impact of COVID-19 has passed in a given geographic area, the consequences of delaying care will almost certainly generate new issues for individuals and the healthcare system, potentially raising annual expenses globally. The pandemic has created an everlasting impact on the market and the healthcare industry.

The scope of our market report is to provide you with top-notch information on the market. The report consists of pie diagrams, bar diagrams, line diagrams, and other infographics to give a holistic and scrutinized view of the dynamic environment of the market. This reports analysis aids players in the business in comprehending shifting market dynamics through time.

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Top key players: Abbott, Roche, Eli Lilly, Johnson and Johnson, GlaxoSmithKline, Lupin, Glenmark, Depomed, Astellas, and Pfizer

Segmentation of Diabetic Neuropathy Treatment Market:

Product Type Coverage

Peripheral Neuropathy

Autonomic Neuropathy

Proximal Neuropathy

Focal Neuropathy

Application Coverage

Hospitals

Clinics

Others

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Diabetic Neuropathy Treatment Market: Regional Segment Analysis

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The report includes six parts, dealing with:1.) Basic information;2.) The Asia Diabetic Neuropathy Treatment Market;3.) The North American Diabetic Neuropathy Treatment Market;4.) The European Diabetic Neuropathy Treatment Market;5.) Market entry and investment feasibility;6.) The report conclusion.

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The Feather and the Knife: Navigating Life With Chronic Pain – POZ

Tuesday, August 17th, 2021

For Jess Guilln, pain is a feather touch and a constant companion. To illustrate, Guilln, who has been living with HIV since 1985, moves one elegant hand, bending at the wrist to mimic running a feather gently along skin.

I just start doing this over and over and over, he says. I tell people, This is a feather. But what do you feel if I keep doing this for 30 minutes, or for an hour?

Usually, folks push him away, irritated at the sensation. Thats one of the ways Guilln describes the chronic pain that sometimes keeps him in bed until noon and can make every step hurt. But thats not the only way he describes it. Theres the feeling of a nail or a thorn from a rose pressed nonstop against skin. And then, theres the pain that wakes him up in the middle of the night and consumes his thoughts, like a knife stabbing him over and over again. For Guilln, chronic pain is a lack of sensation, then, all at once, too much sensationand a sensation he cant escape.

It never stops. [People with chronic pain] dont get used to it, but we manage somehow, he says. We still want to experience life in some way.

Guilln is far from alone. Studies have found that between 25% and 85% of people living with HIV experience chronic pain, compared with estimates of 11% to 20% of the general population. Often, this is neuropathic painpain that starts in the brain but is usually experienced as numbness, tingling, burning or stabbing in the limbs, hands and feet.

Despite the high rates of pain, some research suggests that people living with HIV are less likely to be prescribed opioid pain treatment than their HIV-negative peers. The additional challenge of coexisting substance use disorders can render even that form of pain relief elusive for some people with HIV. But the opioid epidemic has led to new research on pain and how to address it at its core, including specifically for people living with HIV.

What We Know About Pain and HIV

Jessica Robinson-Papp, MD, had just come off a general medicine internship at St. Vincents hospital in New York City, where she fell in love with working with HIV-positive people, when she began training in neurology. Luckily for her, she was able to combine her passions. Today, shes a clinical neurologist at New York Citys Mount Sinai Hospital, serving people with HIV who have a variety of pain syndromes.

The more people with HIV she saw, the more Robinson-Papp realized that peripheral neuropathy was usually just one of a litany of pain complaints her patients had.

Youll start talking about neuropathic pain, she says. And then theyll say, Oh, but then, theres back pain, and Theres pain radiating down, and Theres pain over here, and Then, there are headaches.

What shes learned, and what the science of pain in general has revealed, is that there is no one cause of pain, or, if there is, science hasnt discovered it yet. Its not even clear whether people living with HIV really experience more pain than people without HIV, Robinson-Papp says.

We dont even really know that, she says. Understanding the [source] of pain is very much in its infancy.

We manage somehow. We still want to experience life.

What researchers do know is that pain is more likely a syndromea constellation of symptomsthan one disease with a single cause that can be cured. In fact, each kind of pain could have a different cause.

For instance, neuropathy is often a side effect of older HIV medications or chemotherapy for AIDS-defining illnesses. It could also be due to accelerated aging in people with HIV. Then theres degenerative joint diseasethat is, joint pain due to osteoarthritis or avascular necrosis, which often necessitate joint replacements. For people who menstruate, menopause can come with its own kinds of pain. HIV-associated chronic inflammation is another likely contributor to pain, Robinson-Papp says.

Whats more, people with one pain syndrome, such as HIV-associated peripheral neuropathy, are more likely to have another, like migraines or joint pain from osteoarthritisor even multiple other pain syndromes. Scientists dont know why that is either, says Robinson-Papp.

Plus, some factors may amplify ones perception of pain. For instance, its possible that some HIV viral proteins themselves may enhance pain. Pain is also associated with other health conditions, such as depression, anxiety or posttraumatic stress disorder, most of which can be part of whats known as AIDS Survivor Syndrome, a cluster of symptoms resulting from trauma endured during the early years of the epidemic.

Then there are factors that can make it easier to focus on pain, like the social isolation that can accompany aging. Moreover, certain behaviors, such as lack of exercise, can increase pain, and conditions such as insomnia or drug misuse or addiction (which can be an attempt to self-medicate) can complicate how individuals cope with pain.

All of this can impact the ability to take HIV meds as prescribed, which can deprive people with uncontrolled pain of the health benefits of having an undetectable viral load.

So when Robinson-Papp talks to patients about options to alleviate pain, the first step is to see if theres a physical reason for it, like diabetes, autoimmune diseases, infections such as hepatitis B or C or malnutrition associated with alcoholism.

But once Robinson-Papp has helped patients address those problems, there are only a few proven solutions she can offer people to help manage their pain or at least cope with it. These include physical therapy, massage, acupuncture, mindfulness-based stress reduction, cognitive behavioral therapy, exercise, non-opioid pain relievers and cortisone injections (for joint pain). Some data show that cannabis and capsaicin (derived from chili peppers) alleviated some pain in people with HIV, according to a systematic review published in a recent special issue of the journal AIDS Care on the topic of HIV and chronic pain that Robinson-Papp coedited. But the quality of the data were low, and more work is needed to confirm their effectiveness, researchers wrote.

That leaves one last option. Sometimes people are on opioids, she says. Thats a fact of life.

Guilln knows this all too well. Its taken years to find the right mix of meds, one that keeps the pain to a manageable level but doesnt wallop him with brain fog or fatigue. He rattles off the list of meds hes tried for pain: Cymbalta, morphine, medicines for depression, even schizophrenia drugs.

For five years, hes been on a regimen that works for him: a base of 20 milligrams of OxyContin (oxycodone hydrochloride) twice a day, with Norco (a combination of hydrocodone and acetaminophen) as needed but no more than one pill every four hours. He augments these with over-the-counter pain patches, hot and cold compresses, a device to deliver nerve stimulation to muscles and massagers.

Temperature, movement, vibrationthese are all different elements that affect whatever youre feeling, he says. But this is not a formula or a recipe. It is a lot of work, sadly, to find whatever works for you.

Opioid Epidemic Leads to Innovations

Sciences understanding of HIV and pain may be about to change, however. In the HIV and chronic pain issue of AIDS Care, a global task force of HIV experts began to lay out a research agenda for studying pain in people with HIV. (Their preference: Start with what causes it.) The issue includes new data showing that many HIV-positive people cant separate their chronic pain from their experience of having the virus.

The HIV Global Pain Task Force, of which Robinson-Papp is a member, is now soliciting recommendations for the HIV pain research agenda from people living with HIV.

Another effort is more wide-ranging. The National Institutes of Health (NIH) launched the Helping to End Addiction Long-term (HEAL) Initiative in 2018 and has so far funded it with $1.5 billion to back experimental research and the development of medical devices that might treat opioid use disorder or address or prevent pain.

The funding also supports the Pain Management Effectiveness Research Network, which is testing existing non-opioid drugs against pain, and the Pragmatic and Implementation Studies for the Management of Pain to Reduce Opioid Prescribing as well as new research paths for interventions that could treat pain without requiring opioids.

Thats where Marco Loggia, PhD, associate director of Massachusetts General Hospitals Center for Integrative Pain NeuroImaging, comes in.

Loggia isnt an HIV researcher. But he has dedicated his career to studying what pain of all sorts looks like in the brain using PET and MRI scans.

Neuroinflammation is what brought him to HIV. Chronic HIV infection can lead to persistent immune activation and inflammation even among people on effective antiretroviral treatment who have an undetectable viral load.

Loggias lab was the first to show that in people with chronic pain a protein in the brain called translocator protein (TSPO) is present in unusually high numbers in the thalamus, the part of the brain that perceives pain and other stimuli. If his theory is correct and the presence of TSPO in people with chronic pain isnt just a coincidence but actually an objective marker of how much pain people are in, lowering TSPO might also reduce how much pain a person feels, without the need for opioids. Drugmakers could then develop medications that target and reduce TSPO and therefore reduce the pain itself.

HIV is a perfect storm of neuroinflammation, he says. We wanted to knowabove and beyond the inflammation associated with the viruswhy some people with HIV have pain and some dont.

In short, if all people with HIV have neuroinflammation, why dont they all also have pain? And does neuroinflammation look different in the brains of HIV-positive and HIV-negative people with chronic pain?

Loggias current study is recruiting participants in the Boston area to be part of an imaging study to look at just this. It divides participants into three categories: 30 people living with HIV without chronic pain, 30 people with HIV and chronic pain who engaged in opioid pain management and 30 people with HIV with chronic pain not taking opioids. Thats because of another complication of opioid use: Scientists think ongoing opioid use could actually increase inflammation, and maybe TSPO, in the brain.

The HEAL Initiative gives Robinson-Papp hope for the future of pain treatment for people living with HIV.

The HEAL Initiative has really brought together the addiction world and the pain world, which I think is extraordinarily beneficial, particularly for the pain world, because there are ways addiction medicine conceptualizes care that would be really lovely for us as well, she says, noting addiction cares focus on harm reduction. You have to think about the whole personwhere they live, what the context of their pain is.

Jess GuillnAngela DeCenzo

Reclaiming Joy

One of Guillns early memories as a child was dancing with his aunts. One aunt would take him by the hand, and another aunt would grab his sister. They would teach the kids salsa and other dances. When Guilln remembers it, he beams with adoration for his aunts, one of whom recently died.

In the years since, his experience in his body is, like pain, never just one thing. The breathtaking rush of a first kiss and first touch with another man linger with memories of the burning under his skin that came with his HIV diagnosis. The horror of the feel of bald patches on his scalp from the stress of being closeted and living with HIV in 1985 coexist with the youthful energy of nights spent at discos, dancing until dawn. Theres the mix of adrenaline and the great vibration in his chest from standing in front of a crowd and singing. Now, at 60, in chronic pain and with a hip replacement, Guilln is proud of the fact that these days, when he does dance, he can still break it down all the way to the ground.

Sometimes, when every step on the sidewalk feels like stabbing, he imagines hes walking on a bed of Jell-O. It takes him out of his current body, this painful body that nevertheless he loves.

He can still access the joy he felt dancing as a child. It will cost him in energy and recovery later, but for five or 10 minutes, his feet move in that familiar way, in concert with his shoulders, hips leading, weight shifting from balls of feet to heels, shoulders shifting to compensate. For those minutes, he is that child again, dancing in the kitchen with his aunt.

Some days, thats just a fantasy. But he can escape into that memory and know what its been like to be a whole person in a currently painful body.

Even if were sitting down, we can have those wonderful memories of movement, he says, as his hands come up in front of his chest and his shoulders shimmy. And even with just the hands, or the hands right here, we are in our brains really doing the twist. And it might help.

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The Feather and the Knife: Navigating Life With Chronic Pain - POZ

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Taysha Gene Therapies Secures up to $100 Million Non-Dilutive Term Loan Financing – Yahoo Finance

Tuesday, August 17th, 2021

Financing strengthens balance sheet, furthers financial and operational flexibility and lowers overall cost of capital

No financial covenants and no warrants issued in connection with non-dilutive financing

Full drawdown expected to extend cash runway to support key value-creating milestones including availability of Phase 1/2 GAN data from the highest dose cohort as well as regulatory guidance on registration pathway for GAN, data readouts in GM2 gangliosidosis, Rett syndrome, CLN1 disease, and SURF1-associated Leigh syndrome and, importantly, a potential regulatory approval for TSHA-120 in GAN without the need for additional financing

DALLAS, August 16, 2021--(BUSINESS WIRE)--Taysha Gene Therapies, Inc. (Nasdaq: TSHA), a patient-centric gene therapy company focused on developing and commercializing AAV-based gene therapies for the treatment of monogenic diseases of the central nervous system in both rare and large patient populations, today announced that it has entered into a loan and security agreement with Silicon Valley Bank (SVB) that provides Taysha with up to $100 million of borrowing capacity.

"Access to this non-dilutive financing at an attractive cost of capital, along with the current cash on hand, will provide Taysha with operational and financial flexibility to achieve numerous value-generating milestones including a potential regulatory approval for TSHA-120 in giant axonal neuropathy, or GAN," said RA Session II, Chief Executive Officer of Taysha. "Additional milestones include the release of Phase 1/2 data in the highest dose cohort in GAN, and Phase 1/2 data in GM2 gangliosidosis, Rett syndrome, CLN1 disease and SURF1-associated Leigh syndrome. We are pleased to partner with SVB as we continue to execute on our ambitious business plan."

This non-dilutive financing provides Taysha with up to $100 million, with $40 million available at closing of which Taysha has drawn $30.0 million. The Company has the option to draw down the remaining tranches, subject to certain conditions. The interest rate is the greater of 7.0% or the WSJ Prime Rate plus 3.75%. There are no financial covenants and no warrants associated with the term loan.

Story continues

"Our financial commitment to Taysha speaks to our confidence in its core strategies and is consistent with our support of innovative life sciences businesses," said Michael White, Head of Business Development, Life Science & Healthcare, Silicon Valley Bank. "We are delighted to provide additional capital for the Company to further advance its robust development pipeline and achieve key value-generating milestones in the years to come."

"In the last 12 months, we have quickly made the transition from a private to public company and from preclinical to clinical to pivotal-stage," said Kamran Alam, Chief Financial Officer of Taysha. "Building upon this momentum, we expect this non-dilutive financing to enable us to be well positioned to maximize long-term stockholder value."

About Taysha Gene Therapies

Taysha Gene Therapies (Nasdaq: TSHA) is on a mission to eradicate monogenic CNS disease. With a singular focus on developing curative medicines, we aim to rapidly translate our treatments from bench to bedside. We have combined our teams proven experience in gene therapy drug development and commercialization with the world-class UT Southwestern Gene Therapy Program to build an extensive, AAV gene therapy pipeline focused on both rare and large-market indications. Together, we leverage our fully integrated platforman engine for potential new cureswith a goal of dramatically improving patients lives. More information is available at http://www.tayshagtx.com.

About Silicon Valley Bank

For nearly 40 years, Silicon Valley Bank (SVB) has helped innovative companies and their investors move bold ideas forward, fast. SVB provides targeted financial services and expertise through its offices in innovation centers around the world. With commercial, international and private banking services, SVB helps address the unique needs of innovators. Learn more at svb.com.

Forward-Looking Statements

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Words such as "anticipates," "believes," "expects," "intends," "projects," and "future" or similar expressions are intended to identify forward-looking statements. Forward-looking statements include statements concerning or implying the potential of our product candidates to positively impact quality of life and alter the course of disease in the patients we seek to treat, our research, development and regulatory plans for our product candidates, the anticipated use of proceeds from borrowings under the loan and security agreement, our ability to access the full $100 million potentially available under the loan and security agreement and our ability to fund operations into the second half of 2023. Forward-looking statements are based on managements current expectations and are subject to various risks and uncertainties that could cause actual results to differ materially and adversely from those expressed or implied by such forward-looking statements. Accordingly, these forward-looking statements do not constitute guarantees of future performance, and you are cautioned not to place undue reliance on these forward-looking statements. Risks regarding our business are described in detail in our Securities and Exchange Commission ("SEC") filings, including in our Annual Report on Form 10-K for the year ended December 31, 2020 and our Quarterly Report on Form 10-Q for the quarter ended June 30, 2021, both of which are available on the SECs website at http://www.sec.gov. Additional information will be made available in other filings that we make from time to time with the SEC. Such risks may be amplified by the impacts of the COVID-19 pandemic. These forward-looking statements speak only as of the date hereof, and we disclaim any obligation to update these statements except as may be required by law.

View source version on businesswire.com: https://www.businesswire.com/news/home/20210816005185/en/

Contacts

Company Contact: Kimberly Lee, D.O.SVP, Corporate Communications and Investor RelationsTaysha Gene Therapiesklee@tayshagtx.com

Media Contact: Carolyn HawleyCanale Communicationscarolyn.hawley@canalecomm.com

Read more here:
Taysha Gene Therapies Secures up to $100 Million Non-Dilutive Term Loan Financing - Yahoo Finance

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Sonnet BioTherapeutics Provides Fiscal Year 2021 Third Quarter Business and Earnings Update – Yahoo Finance

Tuesday, August 17th, 2021

Sonnet BioTherapeutics Provides Fiscal Year 2021 Third Quarter Business and Earnings Update

Expanded F H AB Intellectual Property Portfolio

Completed $15.9 million At-The-Market Financing

SON-1010 and SON-080 on track for IND submissions by calendar year end

PRINCETON, NJ / ACCESSWIRE / August 16, 2021 / Sonnet BioTherapeutics Holdings, Inc. (NASDAQ:SONN) ("Sonnet" or the "Company"), a biopharmaceutical company developing innovative targeted biologic drugs, announced today its financial results for the three months ended June 30th , 2021 and provided a business update.

"Throughout the quarter, we've continued to make several advancements towards the clinic with our proprietary Fully Human Albumin Binding (F H AB) pipeline assets, and our partnered product" commented Pankaj Mohan, Ph.D., Founder and CEO. "We are progressing our SON-1010 (F H AB-IL12) and SON-080 (Low-dose IL-6) programs, with IND applications on track to be filed with the FDA for both before the end of 2021, with an additional IND for SON-1210 (IL12-F H AB-IL15) during the first half of 2022. We remain confident that the ability to deliver a therapeutic payload in a more targeted manner than traditional, wild-type cytokines has the potential to result in greater efficacy with an improved toxicity profile."

"We are pleased with our ongoing financing strategy, which is designed to provide the company with the funding necessary to advance our R&D activities and to grow the company beyond 2021," commented Jay Cross, CFO.

FY 2021 Third Quarter and Recent Corporate Updates

Sonnet provided the following corporate updates:

In May 2021, Sonnet entered into a license agreement with New Life Therapeutics, granting exclusive licenses to develop and commercialize SON-080 for the prevention, treatment, or palliation of diabetic peripheral neuropathy in certain territories in Asia.

In June 2021, the United States Patent and Trademark Office issued U.S. Patent No. 11,028,166 entitled "Albumin Domain Fusion Proteins" that covers Sonnet's F H AB technology. The patent also includes therapeutic fusion proteins that utilize F H AB for tumor targeting and retention, thereby providing extended pharmacokinetics.

Story continues

In June 2021, Sonnet executed its final issuance of shares of its common stock under the At-the-Market Sales Agreement, pursuant to which the Company executed issuances of an aggregate of 7,454,238 Shares for aggregate gross proceeds of $15,874,999.

FY 2021 Third Quarter Ended June 30, 2021 Financial Results

As of June 30, 2021, Sonnet had $6.0 million cash on hand.

Research and development expenses were $3.9 million for the three months ended June 30, 2021, compared to $2.5 million for the three months ended June 30, 2020. The increase of $1.4 million was primarily due to increased expenditures for the development of the cell line for IL12-FHAB and IL12-FHAB-IL15 and increased costs for research and development activities due to the acquisition of Relief and an increase in payroll and share-based compensation expense as operations are expanded.

General and administrative expenses were $2.4 million for the three months ended June 30, 2021, compared to $2.5 million for the three months ended June 30, 2020. The decrease of $0.1 million was primarily due to a $0.9 million decrease in professional fees and transaction-related fees associated with the closing of the merger, offset by an increase in payroll and share-based compensation expense of $0.7 million to support expanded operations.

About Sonnet BioTherapeutics Holdings, Inc.

Sonnet BioTherapeutics is an oncology-focused biotechnology company with a proprietary platform for innovating biologic drugs of single or bispecific action. Known as F H AB (Fully Human Albumin Binding), the technology utilizes a fully human single chain antibody fragment (scFv) that binds to and "hitch-hikes" on human serum albumin (HSA) for transport to target tissues. F H AB is the foundation of a modular, plug-and-play construct for potentiating a range of large molecule therapeutic classes, including cytokines, peptides, antibodies and vaccines.

Forward-Looking Statements

This press release contains certain forward-looking statements within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934 and Private Securities Litigation Reform Act, as amended, including those relating to the Company's product development, clinical and regulatory timelines, market opportunity, competitive position, possible or assumed future results of operations, business strategies, potential growth opportunities and other statements that are predictive in nature. These forward-looking statements are based on current expectations, estimates, forecasts and projections about the industry and markets in which the Company operates and management's current beliefs and assumptions.

These statements may be identified by the use of forward-looking expressions, including, but not limited to, "expect," "anticipate," "intend," "plan," "believe," "estimate," "potential, "predict," "project," "should," "would" and similar expressions and the negatives of those terms. These statements relate to future events or the Company's financial performance and involve known and unknown risks, uncertainties, and other factors which may cause actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. Such factors include those set forth in the Company's filings with the Securities and Exchange Commission. Prospective investors are cautioned not to place undue reliance on such forward-looking statements, which speak only as of the date of this press release. The Company undertakes no obligation to publicly update any forward-looking statement, whether as a result of new information, future events or otherwise.

Sonnet Biotherapeutics Investor Contact

Michael V. Morabito, Ph.D.Solebury Trout917-936-8430mmorabito@soleburytrout.com

Sonnet BioTherapeutics Holdings, Inc.Consolidated Balance Sheets(unaudited)

June 30,

September 30,

2021

2020

Assets

Current assets:

Cash

$

6,038,190

$

7,349,903

Prepaid expenses and other current assets

934,213

287,738

Total current assets

6,972,403

7,637,641

Property and equipment, net

58,644

67,889

Operating lease right-of-use asset

144,787

205,919

Other assets

-

82,959

Total assets

$

7,175,834

$

7,994,408

Liabilities and stockholders' equity

Current liabilities:

Related-party notes

$

748

$

21,184

Accounts payable

2,150,791

2,057,559

Accrued expenses

2,508,956

2,063,678

Operating lease liability

91,239

82,060

Deferred income

1,000,000

500,000

Total current liabilities

5,751,734

4,724,481

Note payable

-

124,878

Operating lease liability

55,464

125,132

Total liabilities

5,807,198

4,974,491

Stockholders' equity:

Preferred stock; $0.0001 par value: 5,000,000 shares authorized. No shares issued or outstanding

-

-

Common stock; $0.0001 par value: 125,000,000 shares authorized; 24,757,847 and 14,724,105 issued and outstanding at June 30, 2021 and September 30, 2020, respectively

2,475

1,472

Additional paid-in capital

56,103,306

39,723,702

Accumulated deficit

(54,737,145

)

Excerpt from:
Sonnet BioTherapeutics Provides Fiscal Year 2021 Third Quarter Business and Earnings Update - Yahoo Finance

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