StemCell Therapy

Purpose: Diabetic peripheral neuropathy (DPN) is the commonest cause of neuropathy worldwide, and its prevalence increases with the duration of diabetes. It affects approximately half of patients with diabetes. DPN is symmetric and predominantly sensory, starting distally and gradually spreading proximally in a glove-and-stocking distribution. It causes substantial morbidity and is associated with increased mortality. The unrelenting nature of pain in this condition can negatively affect a patient's sleep, mood, and functionality and result in a poor quality of life. The purpose of this review was to critically review the current literature on the diagnosis and treatment of DPN, with a focus on the treatment of neuropathic pain in DPN.

Methods: A comprehensive literature review was undertaken, incorporating article searches in electronic databases (EMBASE, PubMed, OVID) and reference lists of relevant articles with the authors' expertise in DPN. This review considers seminal and novel research in epidemiology; diagnosis, especially in relation to novel surrogate end points; and the treatment of neuropathic pain in DPN. We also consider potential new pharmacotherapies for painful DPN.

Findings: DPN is often misdiagnosed and inadequately treated. Other than improving glycemic control, there is no licensed pathogenetic treatment for diabetic neuropathy. Management of painful DPN remains challenging due to difficulties in personalizing therapy and ascertaining the best dosing strategy, choice of initial pharmacotherapy, consideration of combination therapy, and deciding on defining treatment for poor analgesic responders. Duloxetine and pregabalin remain first-line therapy for neuropathic pain in DPN in all 5 of the major published guidelines by the American Association of Clinical Endocrinologists, American Academy of Neurology, European Federation of Neurological Societies, National Institute of Clinical Excellence (United Kingdom), and the American Diabetes Association, and their use has been approved by the US Food and Drug Administration.

Implications: Clinical recognition of DPN is imperative for allowing timely symptom management to reduce the morbidity associated with this condition.

Keywords: diabetes; diagnosis; epidemiology; neuropathy; pharmacotherapy.

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Diabetic Peripheral Neuropathy: Epidemiology, Diagnosis, and ... - PubMed

What is auditory neuropathy?

Auditory neuropathy is a hearing disorder in which the inner ear successfully detects sound, but has a problem with sending sound from the ear to the brain. It can affect people of all ages, from infancy through adulthood. The number of people affected by auditory neuropathy is not known, but current information suggests that auditory neuropathies play a substantial role in hearing impairments and deafness.

When their hearing sensitivity is tested, people with auditory neuropathy may have normal hearing or hearing loss ranging from mild to severe. They always have poor speech-perception abilities, meaning that they have trouble understanding speech clearly. People with auditory neuropathy have greater impairment in speech perception than hearing health experts would predict based upon their degree of hearing loss on a hearing test. For example, a person with auditory neuropathy may be able to hear sounds, but would still have difficulty recognizing spoken words. Sounds may fade in and out or seem out of sync for these individuals.

Researchers report several causes of auditory neuropathy. In some cases, the cause may involve damage to the inner hair cellsspecialized sensory cells in the inner ear that transmit information about sounds through the nervous system to the brain. In other cases, the cause may involve damage to the auditory neurons that transmit sound information from the inner hair cells to the brain. Other possible causes may include inheriting genes with mutations or suffering damage to the auditory system, either of which may result in faulty connections between the inner hair cells and the auditory nerve (the nerve leading from the inner ear to the brain), or damage to the auditory nerve itself. A combination of these problems may occur in some cases.

Outer hair cells help amplify sound vibrations entering the inner ear from the middle ear. When hearing is working normally, the inner hair cells convert these vibrations into electrical signals that travel as nerve impulses to the brain, where the brain interprets the impulses as sound.

Although outer hair cellshair cells next to and more numerous than inner hair cellsare generally more prone to damage than inner hair cells, outer hair cells seem to function normally in people with auditory neuropathy.

There are several ways that children may acquire auditory neuropathy. Some children diagnosed with auditory neuropathy experienced particular health problems before or during birth or as newborns. These problems include inadequate oxygen supply during or prior to birth, premature birth, jaundice, low birth weight, and dietary thiamine deficiency. In addition, some drugs used to treat pregnant women or newborns may damage the babys inner hair cells, causing auditory neuropathy. Adults may also develop auditory neuropathy along with age-related hearing loss.

Auditory neuropathy runs in some families, and in some cases, scientists have identified genes with mutations that compromise the ears ability to transmit sound information to the brain. Thus, inheritance of mutated genes is also a risk factor for auditory neuropathy.

Some people with auditory neuropathy have neurological disorders that also cause problems outside of the hearing system. Examples of such disorders are Charcot-Marie-Tooth syndrome and Friedreichs ataxia.

Health professionalsincluding otolaryngologists (ear, nose, and throat doctors), pediatricians, and audiologistsuse a combination of methods to diagnose auditory neuropathy. These include tests of auditory brainstem response (ABR) and otoacoustic emissions (OAE). The hallmark of auditory neuropathy is an absent or very abnormal ABR reading together with a normal OAE reading. A normal OAE reading is a sign that the outer hair cells are working normally.

An ABR test uses electrodes placed on a persons head and ears to monitor brain wave activity in response to sound. An OAE test uses a small, very sensitive microphone inserted into the ear canal to monitor the faint sounds produced by the outer hair cells in response to auditory stimulation. ABR and OAE testing are painless and can be used for newborn babies and infants as well as older children and adults. Other tests may also be used as part of a comprehensive evaluation of an individuals hearing and speech-perception abilities.

Some newborn babies who have been diagnosed with auditory neuropathy improve and start to hear and speak within a year or two. Other infants stay the same, while some get worse and show signs that the outer hair cells no longer function (abnormal otoacoustic emissions). In people with auditory neuropathy, hearing sensitivity can remain stable, get better or worse, or gradually worsen, depending on the underlying cause.

Researchers are still seeking effective treatments for people with auditory neuropathy. Meanwhile, professionals in the hearing field differ in their opinions about the potential benefits of hearing aids, cochlear implants, and other technologies for people with auditory neuropathy. Some professionals report that hearing aids and personal listening devices such as frequency modulation (FM) systems are helpful for some children and adults with auditory neuropathy. Cochlear implants (electronic devices that compensate for damaged or nonworking parts of the inner ear) may also help some people with auditory neuropathy. No tests are currently available, however, to determine whether an individual with auditory neuropathy might benefit from a hearing aid or cochlear implant.

Debate also continues about the best ways to educate and improve communication skills in infants and children who have hearing impairments such as auditory neuropathy. One approach favors sign language as the childs first language. A second approach encourages the use of listening skillstogether with technologies such as hearing aids and cochlear implantsand spoken language. A combination of these two approaches may also be used. Some health professionals believe it may be especially difficult for children with auditory neuropathy to learn to communicate only through spoken language because their ability to understand speech is often severely impaired. Adults with auditory neuropathy and older children who have already developed spoken language may benefit from learning how to speechread (also known as lip reading).

Scientists have identified genes involved in causing some cases of auditory neuropathy, and are working to identify what goes wrong in the auditory system when a person inherits a mutant gene. Researchers are also continuing to investigate the potential benefits of cochlear implants for children with auditory neuropathy, and are examining why cochlear implants may benefit some people with the condition but not others.

The NIDCD maintains a directory of organizations that provide information on the normal and disordered processes of hearing, balance, taste, smell, voice, speech, and language.

NIDCD Information Clearinghouse1 Communication AvenueBethesda, MD 20892-3456Toll-free voice: (800) 241-1044Toll-free TTY: (800) 241-1055Email: nidcdinfo@nidcd.nih.gov

NIH Pub. No. 03-5343September 2016

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What Is Auditory Neuropathy? Causes & Treatment | NIDCD

Vero Neuropathy and Their Patients Pain Free Success Stories | Paid Content  Local 5 - weareiowa.com

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Vero Neuropathy and Their Patients Pain Free Success Stories | Paid Content - Local 5 - weareiowa.com

Neuropathy No More Reviews (Blue Heron Health News) Does It Work?  Outlook India

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Neuropathy No More Reviews (Blue Heron Health News) Does It Work? - Outlook India

This report segments the neuropathy pain treatment market by indication (diabetic neuropathy, chemotherapy-induced neuropathy pain, postherpetic neuralgia, and others) and geography (North America, Europe, APAC, South America, and Middle East and Africa)

NEW YORK, Oct. 4, 2022 /PRNewswire/ -- One of the key trends in the neuropathy pain treatment market growth is the growing focus on emerging economies. Research institutes and vendors are focusing on tapping potential treatments in emerging economies, which will bring substantial growth opportunities. The increasing number of individuals requiring pain treatment has increased the demand for neuropathy pain treatment in countries such as China, India, and Brazil. Research institutes have also issued guidelines to address unmet needs in the treatment of pain. For instance, in APAC, a group of pain specialists has created tailored guidelines for each region. In addition, vendors are establishing new units in emerging economies such as Brazil to expand their presence in the market. Such initiatives will drive market growth during the forecast period.

Technavio has announced its latest market research report titled Global Neuropathy Pain Treatment Market 2022-2026

The global neuropathy pain treatment market size is expected to grow by USD 3.81 billion between 2021 to 2026. In addition, the growth momentum of the market will accelerate at a CAGR of 9.18%, according to Technavio's latest market report.

Get a comprehensive report summary that describes the market size and forecast along with research methodology. The FREE sample reportis available in PDF format

Neuropathy Pain Treatment Market: Market Segmentation

By indication, the diabetic neuropathy segment will be the largest contributor to market growth during the forecast period. Most of the currently approved therapies provide only symptomatic relief. Hence, there is a need for disease-modifying treatments that might slow, prevent, or reverse the progression of nerve damage. Vendors are extensively focusing on R&D activities to address this unmet medical need. For instance, in January 2019, Daiichi Sankyo Company received marketing approval in Japan for the Tarlige drug for the treatment of peripheral neuropathic pain.

Story continues

In terms of geography, North America will present significant opportunities for market vendors due to the factors such as the growing prevalence of diabetes. The region will account for 33% of the market's growth during the forecast period. Moreover, market growth in this region will be faster than the growth of the market in other regions. The US and Canada are the key countries for the neuropathy pain treatment market in North America.

Neuropathy Pain Treatment Market: Major Growth Drivers

The focus on the development of novel therapeutics for postherpetic neuralgia is driving the neuropathy pain treatment market growth. Postherpetic neuralgia is a complication of shingles caused by the chickenpox virus. There are various drugs for the treatment of postherpetic neuralgia. However, the lack of effective therapeutics has negatively impacted the adoption rates. Therefore, vendors are focusing on the development of potential alternatives. Currently, there are around nine molecules for the treatment of postherpetic neuralgia in different stages of development. Such developments will fuel the growth of the global neuropathy pain treatment market growth during the forecast period.

Technavio has identified key trends, drivers, and challenges in the market, which will help vendors improve their strategies to stay ahead of their competitors. View our FREE PDF Sample Report

Neuropathy Pain Treatment Market: Key Vendors

Abbott Laboratories, Assertio Therapeutics Inc., Astellas Pharma Inc., AstraZeneca Plc, Aurobindo Pharma Ltd., Baxter International Inc., Biogen Inc., Bristol Myers Squibb Co., Dr. Reddys Laboratories Ltd, Eli Lilly, and Co., Endo International Plc, GlaxoSmithKline Plc, Johnson and Johnson, Mallinckrodt Plc, Novartis AG, Pfizer Inc., Sanofi SA, Sun Pharmaceutical Industries Ltd, VistaGen Therapeutics Inc., among others, are the main players in the market.

Neuropathy Pain Treatment Market: Reasons to Buy Our Report

CAGR of the market during 2022-2026

Detailed information on factors that will help the neuropathy pain treatment market grow during the next five years

Approximation of the neuropathy pain treatment market size and its contribution to the parent market

Forecasts on upcoming trends and changes in consumer behavior

The growth of the neuropathy pain treatment market across North America, Europe, APAC, South America, and Middle East and Africa

Analysis of the market's competitive landscape and detailed information on vendors

Comprehensive details of factors that will challenge the growth of neuropathy pain treatment market vendors

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Neuropathy Pain Treatment Market Scope

Report Coverage

Details

Page number

120

Base year

2021

Forecast period

2022-2026

Growth momentum & CAGR

Accelerate at a CAGR of 9.18%

Market growth 2022-2026

USD 3.81 billion

Market structure

Fragmented

YoY growth (%)

11.03

Regional analysis

North America, Europe, APAC, South America, and Middle East and Africa

Performing market contribution

North America at 33%

Key consumer countries

US, Canada, India, Germany, and UK

Competitive landscape

Leading companies, competitive strategies, consumer engagement scope

Companies profiled

Abbott Laboratories, Assertio Therapeutics Inc., Astellas Pharma Inc., AstraZeneca Plc, Aurobindo Pharma Ltd., Baxter International Inc., Biogen Inc., Bristol Myers Squibb Co., Dr Reddys Laboratories Ltd, Eli Lilly and Co., Endo International Plc, GlaxoSmithKline Plc, Johnson and Johnson, Mallinckrodt Plc, Novartis AG, Pfizer Inc., Sanofi SA, Sun Pharmaceutical Industries Ltd, and VistaGen Therapeutics Inc.

Market Dynamics

Parent market analysis, market growth inducers and obstacles, fast-growing and slow-growing segment analysis, COVID-19 impact and future consumer dynamics, and market condition analysis for the forecast period.

Customization purview

If our report has not included the data that you are looking for, you can reach out to our analysts and get segments customized.

Browse Health CareMarket Reports

Table of Contents

1 Executive Summary

2 Market Landscape

3 Market Sizing

4 Five Forces Analysis

5 Market Segmentation by Indication

6 Customer Landscape

7 Geographic Landscape

8 Drivers, Challenges, and Trends

9 Vendor Landscape

10 Vendor Analysis

11 Appendix

About Us

Technavio is a leading global technology research and advisory company. Their research and analysis focus on emerging market trends and provide actionable insights to help businesses identify market opportunities and develop effective strategies to optimize their market positions. With over 500 specialized analysts, Technavio's report library consists of more than 17,000 reports and counting, covering 800 technologies, spanning across 50 countries. Their client base consists of enterprises of all sizes, including more than 100 Fortune 500 companies. This growing client base relies on Technavio's comprehensive coverage, extensive research, and actionable market insights to identify opportunities in existing and potential markets and assess their competitive positions within changing market scenarios.

ContactTechnavio ResearchJesse MaidaMedia & Marketing ExecutiveUS: +1 844 364 1100UK: +44 203 893 3200Email: media@technavio.comWebsite: http://www.technavio.com/

Global Neuropathy Pain Treatment Market 2022-2026

Cision

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Neuropathy Pain Treatment Market Size to Grow by USD 3.81 Bn, Growing Focus on Emerging Economies to be a Key Trend - Technavio - Yahoo Finance

NEW YORK, Oct. 5, 2022 /PRNewswire/ -- The Global Pregabalin Market by Application and Geography Forecast and Analysis 2022-2026 size is expected to grow by USD 153.03 million from 2022 to 2026, at a CAGR of 3.74%. The increasing presence of a large patient pool related to neuropathic pain, the increasing geriatric population, and the rising applications of pregabalin in various diseases are themajor factors propelling the market growth. However, the growing preference for alternatives and stringent regulatory policies may impede market growth. To get more insights on drivers and challenges Request a Sample PDF

Technavio has announced its latest market research report titled Global Pregabalin Market 2022-2026

Key Market Dynamics:

Market Driver: The presence of a large patient pool related to neuropathic pain is one of the key drivers supporting thepregabalin market growth.Neuropathic pain is associated with various disorders such as diabetic neuropathy, chemotherapy-induced pain, shingles, and herniated disk. There have been growing cases of these disorders, especially in the geriatric population. Meanwhile, the increasing number of individuals preferring chemotherapy for cancer treatment is fueling cases of chemotherapy-induced pain. Furthermore, according to the CDC, the incidence of shingles is approximately four per 1,000 US population annually. Overall, there are an estimated one million cases of herpes zoster in the US annually. Such a scenario will lead to an increase in the adoption of pregabalin, which, in turn, will drive the growth of the market during the forecast period.

Market Challenges: Growing preference for alternatives is one of the key factors hindering thepregabalin market growth.As the current treatments are associated with many unmet needs, end-users are looking to shift to alternative therapies. For instance, diabetic neuropathic pain can be reduced by supplementing essential acids, alpha-lipoic acid, gamma-linolenic acid, and omega-3 fatty acids. Similarly, acupuncture can be an effective way to manage peripheral neuropathy. Acupuncture uses pressure points across the body to realign the body's energy.Thus, the use of these alternative therapies may hinder growth prospects in the forecast period.

To get insights about additional key drivers, trends, and challenges available with Technavio.Read our Sample Report right now!

Market Segmentation

North Americawill be the leading region with 36% of the market's growth during the forecast period. The US and Canada are the key countries for the pregabalin market inNorth America. The increase in the older population, coupled with the established adoption of LYRICA and Cymbalta in new indications and the introduction of new drugs for the treatment of neuropathic pain, will facilitate thepregabalin market growth in North America over the forecast period.

The Neuropathic pain application segment will contribute the highest market share growth during the forecast period. Neuropathic pain affects 20% to 30% of diabetic neuropathy patients. Thus, the demand for pregabalin is rising due to more occurrences of diabetic neuropathy, which is boosting the growth of the market.Pregabalin is an alternative treatment for people with neuropathic pain that has not responded to other drugs.It effectively reduces the symptoms of numerous neuropathic pain conditions and positions itself as a first-line therapy option with exceptional safety and efficacy.These factors will drive segment growth during the forecast period.

View our sample reportfor additional insights into the contribution of all the segments, and regional opportunities in the report.

Some Companies Mentioned with their Offerings

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Pregabalin Market Scope

Report Coverage

Details

Page number

120

Base year

2021

Forecast period

2022-2026

Growth momentum & CAGR

Accelerate at a CAGR of 3.74%

Market growth 2022-2026

USD 153.03 million

Market structure

Fragmented

YoY growth (%)

3.27

Regional analysis

North America, Europe, Asia, and Rest of World (ROW)

Performing market contribution

North America at 36%

Key consumer countries

US, Canada, Germany, China, Japan, and Republic of Korea

Competitive landscape

Leading companies, competitive strategies, consumer engagement scope

Companies profiled

Biomax Biotechnics Pvt.Ltd., Camber Pharmaceuticals Inc., Cipla Ltd., Dr. Kumars Pharmaceuticals, Genesis Biotec Inc., H. L. Healthcare Pvt. Ltd., Lupin Ltd, Medley Pharmaceuticals Ltd., MK Medicine, MSN Laboratories, Neuracle Lifesciences Pvt. Ltd., Novartis AG, Pfizer Inc., Phoenix Biologicals Pvt. Ltd., Sun Pharmaceutical Industries Ltd, Swastik Life Sciences, Torrent Pharmaceuticals Ltd., and Vibcare Pharma Pvt. Ltd.

Market Dynamics

Parent market analysis, Market growth inducers and obstacles, Fast-growing and slow-growing segment analysis, COVID-19 impact and future consumer dynamics, and market condition analysis for the forecast period.

Customization purview

If our report has not included the data that you are looking for, you can reach out to our analysts and get segments customized.

Table of Contents:

1 Executive Summary

2 Market Landscape

3 Market Sizing

4 Five Forces Analysis

5 Market Segmentation by Application

6 Customer Landscape

7 Geographic Landscape

8 Drivers, Challenges, and Trends

9 Vendor Landscape

10 Vendor Analysis

11 Appendix

About Us

Technavio is a leading global technology research and advisory company. Their research and analysis focuses on emerging market trends and provides actionable insights to help businesses identify market opportunities and develop effective strategies to optimize their market positions.

With over 500 specialized analysts, Technavio's report library consists of more than 17,000 reports and counting, covering 800 technologies, spanning across 50 countries. Their client base consists of enterprises of all sizes, including more than 100 Fortune 500 companies. This growing client base relies on Technavio's comprehensive coverage, extensive research, and actionable market insights to identify opportunities in existing and potential markets and assess their competitive positions within changing market scenarios.

ContactTechnavio ResearchJesse MaidaMedia & Marketing ExecutiveUS: +1 844 364 1100UK: +44 203 893 3200Email:media@technavio.comWebsite:www.technavio.com/

Global Pregabalin Market 2022-2026

Cision

View original content to download multimedia:https://www.prnewswire.com/news-releases/pregabalin-market-to-grow-by-usd-153-03-mn-from-2022-to-2026--driven-by-presence-of-large-patient-pool-related-to-neuropathic-pain---technavio-301640610.html

SOURCE Technavio

Read more:
Pregabalin Market to Grow by USD 153.03 Mn from 2022 to 2026, Driven by Presence of Large Patient Pool Related To Neuropathic Pain - Technavio - Yahoo...

Feldman, E. L., Nave, K., Jensen, T. S. & Bennett, D. L. H. New horizons in diabetic neuropathy: Mechanisms, bioenergetics, and pain. Neuron 93, 12961313 (2017).

CAS PubMed PubMed Central Google Scholar

Callaghan, B. C., Cheng, H. T., Stables, C. L., Smith, A. L. & Feldman, E. L. Diabetic neuropathy: Clinical manifestations and current treatments. Lancet Neurol. 11, 521534 (2012).

PubMed PubMed Central Google Scholar

Jensen, T. S. & Finnerup, N. B. Allodynia and hyperalgesia in neuropathic pain: Clinical manifestations and mechanisms. Lancet Neurol. 13, 924935 (2014).

PubMed Google Scholar

Truini, A., Garcia-Larrea, L. & Cruccu, G. Reappraising neuropathic pain in humansHow symptoms help disclose mechanisms. Nat. Rev. Neurol. 9, 572582 (2013).

CAS PubMed Google Scholar

Gandhi, R. A. & Selvarajah, D. Understanding and treating painful diabetic neuropathy: Time for a paradigm shift. Diabet. Med. 32, 771777 (2015).

CAS PubMed Google Scholar

Harris, K., Boland, C., Meade, L. & Battise, D. Adjunctive therapy for glucose control in patients with type 1 diabetes. Diabetes Metab. Syndr. Obes. 11, 159173 (2018).

CAS PubMed PubMed Central Google Scholar

Yagihashi, S., Mizukami, H. & Sugimoto, K. Mechanism of diabetic neuropathy: Where are we now and where to go?. J. Diabetes Investig. 2, 1832 (2011).

CAS PubMed Google Scholar

Lee, A. Y. & Chung, S. S. Contributions of polyol pathway to oxidative stress in diabetic cataract. FASEB J. 13, 2330 (1999).

CAS PubMed Google Scholar

Brownlee, M. Biochemistry and molecular cell biology of diabetic complications. Nature 414, 813820 (2001).

ADS CAS PubMed Google Scholar

Yan, L.-J. Pathogenesis of chronic hyperglycemia: From reductive stress to oxidative stress. J. Diabetes Res. 2014, 137919 (2014).

PubMed PubMed Central Google Scholar

Schreiber, A. K., Nones, C. F. M., Reis, R. C., Chichorro, J. G. & Cunha, J. M. Diabetic neuropathic pain: Physiopathology and treatment. World J. Diabetes. 6, 432444 (2015).

PubMed PubMed Central Google Scholar

Thornalley, P. J. Glycation in diabetic neuropathy: Characteristics, consequences, causes, and therapeutic options. Int. Rev. Neurobiol. 50, 3757 (2002).

CAS PubMed Google Scholar

Juranek, J., Ray, R., Banach, M. & Rai, V. Receptor for advanced glycation end-products in neurodegenerative diseases a bad reputation. Rev. Neurosci. 26, 691698 (2015).

PubMed Google Scholar

Greene, D. A., Stevens, M. J., Obrosova, I. & Feldman, E. L. Glucose-induced oxidative stress and programmed cell death in diabetic neuropathy. Eur. J. Pharmacol. 375, 217223 (1999).

CAS PubMed Google Scholar

Pop-Busui, R., Sima, A. & Stevens, M. Diabetic neuropathy and oxidative stress. Diabetes Metab. Res. Rev. 22, 257273 (2006).

CAS PubMed Google Scholar

Ishii, D. N. & Lupien, S. B. Insulin-like growth factors protect against diabetic neuropathy: Effects on sensory nerve regeneration in rats. J. Neurosci. Res. 40, 138144 (1995).

CAS PubMed Google Scholar

Fernyhough, P. & Calcutt, N. A. Abnormal calcium homeostasis in peripheral neuropathies. Cell Calcium 47, 130139 (2010).

CAS PubMed Google Scholar

Koya, D. et al. Characterization of protein kinase C beta isoform activation on the gene expression of transforming growth factor-beta, extracellular matrix components, and prostanoids in the glomeruli of diabetic rats. J. Clin. Investig. 100, 115126 (1997).

CAS PubMed PubMed Central Google Scholar

Akude, E. et al. Diminished superoxide generation is associated with respiratory chain dysfunction and changes in the mitochondrial proteome of sensory neurons from diabetic rats. Diabetes 60, 288297 (2011).

CAS PubMed Google Scholar

Chowdhury, S. K. R. et al. Mitochondrial respiratory chain dysfunction in dorsal root ganglia of streptozotocin-induced diabetic rats and its correction by insulin treatment. Diabetes 59, 10821091 (2010).

CAS PubMed PubMed Central Google Scholar

Younger, D. S., Rosoklija, G., Hays, A. P., Trojaborg, W. & Latov, N. Diabetic peripheral neuropathy: A clinicopathologic and immunohistochemical analysis of sural nerve biopsies. Muscle Nerve. 19, 722727 (1996).

CAS PubMed Google Scholar

Tomlinson, D. R. & Gardiner, N. J. Diabetic neuropathies: Components of etiology. J. Peripher. Nerv. Syst. 13, 112121 (2008).

CAS PubMed Google Scholar

Satoh, J., Yagihashi, S. & Toyota, T. The possible role of tumor necrosis factor- in diabetic polyneuropathy. Exp. Diabesity Res. 4, 6571 (2003).

PubMed PubMed Central Google Scholar

Yamagishi, S.-I. et al. Correction of protein kinase C activity and macrophage migration in peripheral nerve by pioglitazone, peroxisome proliferator activated-gamma-ligand, in insulin-deficient diabetic rats. J. Neurochem. 104, 491499 (2008).

CAS PubMed Google Scholar

Du, Y. et al. Effects of p38 MAPK inhibition on early stages of diabetic retinopathy and sensory nerve function. Investig. Ophthalmol. Vis. Sci. 51, 21582164 (2010).

Google Scholar

Seger, R. & Krebs, E. G. The MAPK signaling cascade. FASEB J. 9, 726735 (1995).

CAS PubMed Google Scholar

Lewis, T. S., Shapiro, P. S. & Ahn, N. G. Signal transduction through MAP kinase cascades. Adv. Cancer Res. 74, 49139 (1993).

Google Scholar

Widmann, C., Gibson, S., Jarpe, M. B. & Johnson, G. L. Mitogen-activated protein kinase: Conservation of a three-kinase module from yeast to human. Physiol. Rev. 79, 143180 (1999).

CAS PubMed Google Scholar

Obata, K. & Noguchi, K. MAPK activation in nociceptive neurons and pain hypersensitivity. Life Sci. 74, 26432653 (2004).

CAS PubMed Google Scholar

Johnson, G. L. & Lapadat, R. Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases. Science 298, 19111912 (2002).

ADS CAS PubMed Google Scholar

Krishna, M. & Narang, H. The complexity of mitogen-activated protein kinases (MAPKs) made simple. Cell Mol. Life Sci. 65, 35253544 (2008).

CAS PubMed Google Scholar

Yang, S.-H., Sharrocks, A. D. & Whitmarsh, A. J. Transcriptional regulation by the MAP kinase signaling cascades. Gene 320, 321 (2003).

CAS PubMed Google Scholar

Bonny, C., Borsello, T. & Zine, A. Targeting the JNK pathway as a therapeutic protective strategy for nervous system diseases. Rev. Neurosci. 67, 5767 (2005).

Google Scholar

Tsuda, M., Ueno, H., Kataoka, A., Tozaki-Saitoh, H. & Inoue, K. Activation of dorsal horn microglia contributes to diabetes-induced tactile allodynia via extracellular signal-regulated protein kinase signaling. Glia 56, 378386 (2008).

PubMed Google Scholar

Wodarski, R., Clark, A. K., Grist, J., Marchand, F. & Malcangio, M. Gabapentin reverses microglial activation in the spinal cord of streptozotocin-induced diabetic rats. Eur. J. Pain 13, 807811 (2009).

CAS PubMed Google Scholar

Manning, A. M. & Davis, R. J. Targeting JNK for therapeutic benefit: From junk to gold?. Nat. Rev. Drug Discov. 2, 554565 (2003).

CAS PubMed Google Scholar

Agell, N., Bachs, O., Rocamora, N. & Villalonga, P. Modulation of the Ras/Raf/MEK/ERK pathway by Ca(2+), and calmodulin. Cell Signal. 4, 649654 (2002).

Google Scholar

White, C. D. & Sacks, D. B. Regulation of MAP kinase signaling by calcium. Methods Mol. Biol. 661, 151165 (2010).

CAS PubMed Google Scholar

Rosen, L. B., Ginty, D. D., Weber, M. J. & Greenberg, M. E. Membrane depolarization and calcium influx stimulate MEK and MAP kinase via activation of Ras. Neuron 12, 12071221 (1994).

CAS PubMed Google Scholar

Purves, T. et al. A role for mitogen-activated protein kinases in the etiology of diabetic neuropathy. FASEB J. 15, 25082514 (2001).

CAS PubMed Google Scholar

Price, S. A., Agthong, S., Middlemas, A. B. & Tomlinson, D. R. Mitogen-activated protein kinase p38 mediates reduced nerve conduction velocity in experimental diabetic neuropathy: Interactions with aldose reductase. Diabetes 53, 18511856 (2004).

CAS PubMed Google Scholar

Tsuda, M., Mizokoshi, A., Shigemoto-Mogami, Y., Koizumi, S. & Inoue, K. Activation of p38 mitogen-activated protein kinase in spinal hyperactive microglia contributes to pain hypersensitivity following peripheral nerve injury. Glia 45, 8995 (2004).

PubMed Google Scholar

Daulhac, L. et al. Diabetes-induced mechanical hyperalgesia involves spinal mitogen-activated protein kinase activation in neurons and microglia via N-methyl-d-aspartate-dependent mechanisms. Mol. Pharmacol. 70, 12461254 (2006).

CAS PubMed Google Scholar

Piao, Z. G. et al. Activation of glia and microglial p38 MAPK in medullary dorsal horn contributes to tactile hypersensitivity following trigeminal sensory nerve injury. Pain 121, 219231 (2006).

CAS PubMed Google Scholar

Xu, J.-T. et al. p38 activation in uninjured primary afferent neurons and in spinal microglia contributes to the development of neuropathic pain induced by selective motor fiber injury. Exp. Neurol. 204, 355365 (2007).

CAS PubMed Google Scholar

Cheng, H.-L. & Feldman, E. L. Bidirectional regulation of p38 kinase and c-Jun N-terminal protein kinase by insulin-like growth factor-I. J. Biol. Chem. 273, 1456014565 (1998).

CAS PubMed Google Scholar

Cheng, C. & Zochodne, D. W. Sensory neurons with activated caspase-3 survive long-term experimental diabetes. Diabetes 52, 23632371 (2003).

CAS PubMed Google Scholar

Vincent, A. M., McLean, L. L., Backus, C. & Feldman, E. L. Short-term hyperglycemia produces oxidative damage and apoptosis in neurons. FASEB J. 19, 638640 (2005).

CAS PubMed Google Scholar

Senning, E. N. & Gordon, S. E. Activity and Ca2+ regulate the mobility of TRPV1 channels in the plasma membrane of sensory neurons. Elife 4, e03819 (2015).

PubMed PubMed Central Google Scholar

Way, K. J., Katai, N. & King, G. L. Protein kinase C and the development of diabetic vascular complications. Diabet. Med. 18, 945959 (2001).

CAS PubMed Google Scholar

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Anti-hyperalgesic effects of photobiomodulation therapy (904 nm) on streptozotocin-induced diabetic neuropathy imply MAPK pathway and calcium dynamics...

Navigating cancer treatment is a challenge unlike any other. Medical professionals often advise cancer patients to lean on their support systems during treatment, and heeding that advice can make it easier to manage the ups and downs that can arise when being treated for cancer.

In addition to building a strong and trustworthy support system, individuals diagnosed with breast cancer can study up on what to expect during treatment. Side effects of treatment may differ depending on the treatment plan devised by womens cancer care teams. Such plans are not uniform, and the National Breast Cancer Foundation, Inc. notes that treatments often include a combination of therapies, including chemotherapy and radiation. In addition, no two women are the same, so they may respond differently to similar treatment plans than others have in the past. Despite the differences between treatment plans and patients, Johns Hopkins Medicine notes that women may experience an assortment of side effects, including:

Fatigue

Headaches

Pain and numbness: The pain and numbness associated with breast cancer treatment is potentially linked to peripheral neuropathy, an umbrella term that the National Institute of Neurological Disorders and Stroke says refers to the many conditions that involve damage to the peripheral nervous system. The NINDS notes that this connection is due to certain chemotherapy drugs and not all patients will develop the pain and numbness associated with peripheral neuropathy.

Dental issues: Among the potential dental issues that can arise during breast cancer treatment are mucositis (severe inflammation of the mouth), an increased risk for oral infections, difficulty swallowing, and pain that feels like a significant toothache, among others.

Lymphedema: Lymphedema is swelling in an arm or leg that the Mayo Clinic notes can be caused by cancer treatments that remove or damage the lymph nodes.

Musculoskeletal symptoms: Issues such as myalgia and muscle stiffness have been reported in a high percentage of patients who underwent aromatase inhibitor therapy for breast cancer.

Bone loss and osteoporosis

Heart problems: Breastcancer.org indicates that various types of treatment, including chemotherapy and targeted therapies, have been found to affect the heart, blood vessels and immune system, potentially increasing the risk for heart attack, stroke and heart failure.

New cancers

Cataracts

Blood clots

Absence of menstrual periods

Menopausal symptoms

Sexual difficulties: WebMD notes that a lack of sex drive, vaginal dryness and pain during intercourse are some of the sexual difficulties that can arise during breast cancer treatment.

Infertility

Concerns about memory loss and cognitive function, which is sometimes referred to as chemo brain Side effects vary during breast cancer treatment. Some women may not experience anything more than minor issues during treatment. But women are urged to discuss side effects with their cancer care teams and seek guidance about how to alleviate or overcome any symptoms that adversely affect their quality of life

Link:
Side effects that may arise during breast cancer treatment The Hamburg Reporter - Hamburg Reporter

Dr. Sarah Yang

Peripheral neuropathy, a condition that refers to damage to the peripheral nervous system, affects an estimated 20 to 30 million Americans per year. The condition can be difficult to diagnose and hard to treat, which has led many neuropathy patients to seek alternative treatments. Banner Health is looking to provide education on the treatments available to northern Colorado residents to not only manage expectations but also help those suffering from neuropathy receive the best care possible.

Symptoms of peripheral neuropathy often start with tingling, numbness, weakness or sensitivity in the hands and feet that can progress up the arms and legs. Because of these symptoms, neuropathy patients can be more prone to falls and they may not feel, and subsequently treat, wounds to the body, putting them at higher risk for infection.

When meeting a new neuropathy patient, Dr. Sarah Yang, a neurologist at Banner Health Center in Fort Collins, starts by trying to understand if there is an underlying cause of her patients neuropathic pain such as a pinched nerve or diabetes. If there is an underlying cause, addressing the issue is the first method of treatment. If there is not, prescribing pain medications is the only treatment available. Peripheral neuropathy isnt known to have any cure, nor is it reversible. It is expected that patients will decline in their condition, which leaves many who suffer from it in a state of frustration.

Some alternative methods such as diet and exercise are valid and beneficial, while others with little validating data, could be misleading or detrimental to patient health. Additionally, these methods often arent covered by insurance, resulting in high out-of-pocket expenses for the patient.

Its hard to live with the idea that this is an incurable disease and that it is going to get worse, Dr. Sarah Yang said. It is imperative that patients seek the advice of a medical professional when considering these new, and often times unregulated, treatment methods.

Alternative treatment methods are becoming more widely sought after and educating the community on what is safe and effective is vital.

Show your support for Local Journalism by helping us do more of it. It's a kind and simple gesture that will help us continue to bring stories like this to you.

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Neuropathy & the Truth About Alternative Care - North Forty News

Megan McKinney-Dyson was shocked when she received a diagnosis of stage 3b colon cancer in 2021. She was just 42 years old and the mother of two young boys. After undergoing surgery and six months of chemotherapy, she is now cancer-free.

However, the treatment left her with neuropathy, which, according to the American Cancer Society, is a condition that causes pain, numbness and tingling in the hands and feet.

Although her doctor warned her that neuropathy was a potential side effect of her treatment, she wasnt fully prepared for long-term pain and discomfort.

Neuropathy is the biggest thing that I still have to this day, McKinney-Dyson says. Its like constant pins and needles. Its very painful.

She tried medication, but it didnt provide the relief she was seeking. In addition, I didnt like the side effects of the medicine because it made me really tired, she says. So McKinneyDyson turned to alternative treatments such as occupational and physical therapy.

The gap in survivorship research means that patients such as McKinney-Dyson often have difficulty getting the care they need after finishing treatment.

Read more: Peripheral Neuropathy Is 'Underestimated' in Patients Undergoing Cancer Treatment

The growing numbers of cancer survivors are outstripping the capacity of cancer care systems to keep pace with demand, Dr. Aisha Ahmed, an oncologist at Arizona Oncology in Tucson, says.

Primary care physicians may not be adequately prepared to care for these survivors due to perceived knowledge gaps about the individualized needs, risks and surveillance plans for cancer survivors, Ahmed says. This is especially true for patients who are living with long-term side effects of their treatment.

Cancer treatment often involves powerful drugs that can damage the nerves, resulting in chemotherapy-induced peripheral neuropathy (CIPN). Although any type of cancer treatment can cause neuropathy, some drugs are more likely to cause the condition.

Certain types of chemotherapy drugs are neurotoxic, says Dr. Kord Kober, an associate professor of physiological nursing at the University of California, San Francisco. Unfortunately, two of the most common types of neurotoxic chemotherapies, platinum and taxane compounds, are used to treat some of the most common cancers breast, gastrointestinal, lung, gynecologic.

The condition can develop during treatment and persist long after treatment has ended. Due to the lack of prospective longitudinal studies that have evaluated the onset and persistence of CIPN, we do not know the recovery rates for CIPN, Kober says.

For McKinney-Dyson, the neuropathy affects the way she uses her hands and feet.

For the longest time I couldnt explain (the sensation), she says. She describes it as the worst feeling youve ever felt, for something you cant feel, meaning that she experiences the sensation of pain even though no physical stimuli are causing it.

McKinney-Dyson, who is an elementary school teacher, has had to adjust the way she does her job. Tying shoes, zipping jackets, buttoning clothes and even writing can be extremely painful. I have to take more frequent breaks when Im writing, she says. Typing is also difficult, and she often relies on her husbands help with many daily tasks.

CIPN is a relatively new field of study, and there is still much unknown about the condition. Kober works to increase awareness and understanding of CIPN to improve patient outcomes.

Results of a study he co-authored and is published in the Journal of Pain and Symptom Management, which focused on paclitaxelinduced peripheral neuropathy in cancer survivors, found that patients treated with paclitaxel chemotherapy had more problems with balance, the function of their upper extremities and more severe symptoms than patients who were not treated with the drug.

Results of the study also showed that those treated with paclitaxel had reduced quality of life scores in both physical and psychological domains.

Another study published in the Journal of Pain and Symptom Management found that body mass index may be a modifiable risk factor for the severity of chemotherapy-induced neuropathy. Research results show that survivors with a higher body mass index had more severe symptoms of neuropathy. This finding is significant because it suggests there may be ways to mitigate the severity of the condition with lifestyle and diet changes.

Mark Kantrowitz, a survivor of stage 3 testicular seminoma and author of Tumor Humor: Cancer Jokes and Anecdotes, has CIPN, even though it has been nearly two decades since his treatment ended.

After performing a self-exam at home in 2003 at the age of 36, Kantrowitz

found a lump on his testicle. His doctor scheduled an ultrasound for two weeks later, and the results confirmed that the mass was cancerous.

Kantrowitz began treatment immediately. He underwent orchiectomy surgery to remove his testicles and three cycles of chemotherapy and was treated with a combination of bleomycin, etoposide and cisplatin. He credits his research skills for helping him understand his diagnosis and treatment options throughout the process.

Aside from his longterm CIPN, Kantrowitz experienced many rare side effects and complications, including chemo-induced pancreatitis and gallstones, high-pitch hearing loss, Raynauds phenomenon (decreased blood flow in the fingers) and diabetes.

The neuropathy has caused him to experience numbness and tingling in his hands and feet, as well as muscle weakness. His symptoms are very noticeable when he walks, and he uses a cane to get around.

In my case, it mostly affected my feet, though occasionally it would affect the first three fingers on each hand, he says.

Its like wearing a pair of gloves on my feet, Kantrowitz says of the sensation. At the same time,there is a burning and tingling sensation, sometimes really severe. He describes the feeling as being similar to when the foot falls asleep and then begins to wake up. Multiply that by 10 and thats the sensation of neuropathy I experience, he says.

According to research published by the American Society of Clinical Oncology (ASCO), the effects of CIPN can last for years. Of 986 respondents to a 2020 ASCO survey, 77% reported current symptoms of CIPN, with the average respondent being more than three years post treatment.

McKinney-Dyson and Kantrowitz discovered ways to cope with their CIPN. McKinney-Dyson has made changes to her lifestyle and the way she completes everyday tasks. Although she didnt do well with the medication, six weeks of occupational and physical therapy helped her gain back some of the function shed lost.

For patients with cancer who are experiencing CIPN following treatment, there are some prescription medications that can be used to improve symptoms. One of them is duloxetine, Ahmed says. According to Kober, duloxetine is the only proven treatment for CIPN, but there are limited benefits to taking the medication.

Gabriela Miller, an oncology physiotherapist and owner of ACE Cancer Rehab in Mission, Kansas, works with cancer survivors before, during and after chemotherapy to help them manage treatment side effects such as neuropathy. She recommends patients with CIPN start by working with a physical therapist experienced in cancer-related side effects to help them regain function and strength as soon as possible.

CIPN is a very real and common side effect following chemotherapy that can have a huge impact on patients quality of life, Miller says. People who experience neuropathy have decreased sensation and circulation in their feet, which puts them at risk for falling or sustaining a soft tissue injury. If the foot is injured, they run the risk of not feeling the injury, which can potentially make the wound worse.

The effect that CIPN has on a patients life can be profound, with many risks and dangers that are often overlooked.

Another danger is increased risk of falling since the balance and sensation are impaired. We also see decreased muscle strength in the muscles of the toes, which further increases fall risk, Miller says.

Miller suggests patients with cancer consult with an oncology physical therapist as early as possible even before treatment starts. This way, we can detect and manage symptoms of neuropathy and educate the person on what to look for and how to improve their sensation and balance, she says.

She emphasizes that exercises to improve circulation and sensation, as well as balance training, are important components of therapy. Learning how to manage symptoms and risks prevent falls or other injuries associated with this neuropathy.

Kantrowitz, who did not take medication for his CIPN symptoms, found that there is no one-size-fits-all solution. Although he also has issues with daily tasks such as typing, he relies on proofreading software and spelling algorithms to help him. When asked what lifestyle changes have helped alleviate his symptoms, Kantrowitz says, Nothing really helps.

Despite that, having a positive attitude and high pain tolerance have boosted him through some of the darkest days.

Ive learned that I can work through the pain, he says. I have a constant burning sensation in my feet 24/7. He frequently uses distraction techniques to take his mind off the discomfort. Hes learned that his mind is a powerful tool for overcoming many obstacles, including neuropathy. If I dont focus on it, I can ignore it, he says.

Kantrowitz and McKinney-Dyson both agree that the lifesaving treatment was worth the side effects.

In my cancer joke book, Tumor Humor, I joke that its better to be alive with side effects than dead without, Kantrowitz says. I still would have had the same treatment. There really isnt anything I could have done differently.

There is much to learn about CIPN and scientists are working hard to find new ways to prevent and treat the side effect. Ahmed and Kober are hopeful that new medications and treatments will be developed to help those with this debilitating condition. Several ongoing clinical trials are testing new and advanced therapies.

In terms of pharmacology, there are numerous clinical trials under way to evaluate for drug therapeutics to prevent and treat CIPN, Kober says.

Scrambler therapy is one of the pain management techniques being studied. It uses electrical stimulation to scramble the pain signals being sent from the nerves to the brain. Although the study is still in the early phase, Ahmed is optimistic about the treatments potential.

Scrambler therapy is an emerging treatment approach that appears to benefit some affected patients with CIPN, she says. Small studies have suggested that scrambler therapy can reduce chemotherapy-induced neuropathy symptoms, even if symptoms have been present for more than one year.

Its a small ray of hope and something that patients such as McKinney-Dyson and Kantrowitz can hold on to. Kantrowitz recommends other survivors speak to their doctor about any side effects they may be experiencing, even years after treatment has ended.

For more news on cancer updates, research and education, dont forget tosubscribe to CUREs newsletters here.

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Chemotherapy-Induced Peripheral Neuropathy: The Invisible Side Effect - Curetoday.com

Mice

We used 510-week-old C57BL/6NCr male mice (SLC, Shizuoka, Japan) as the wild type (WT), and TRPV1-deficient (TRPV1/) and TRPA1-deficient (TRPA1/) male mice maintained on a C57BL/6NCr background46. Mice were housed in standard cages and maintained under a 12-h light/dark cycle at an ambient temperature of 242C with access to food and water ad libitum. All the animal care and experimental procedures were approved by our Institutional Animal Care and Use Committee and followed the National Institutes of Health and National Institute for Physiological Sciences guidelines (21A008), and carried out in compliance with the ARRIVE guidelines.

Diabetes was induced in mice by administering a single intraperitoneal dose of 150mg/kg STZ (Sigma-Aldrich) prepared freshly in 0.02M citrate buffer (pH 4.5) after a 24-h fasting period when they became 5weeks old. WT (non-DM), TRPV1/ (non-DM) and TRPA1/ (non-DM) mice received an equal volume of citrate-buffer vehicle. One week after administering STZ, the mice with consequent blood glucose concentrations of >400mg/dL were selected as WT (DM), TRPV1/ (DM) and TRPA1/ (DM) mice. Blood glucose levels were measured by Glutest Neo (Sanwa Kagaku Kenkyusho, Nagoya, Japan). Serum insulin concentration was measured by collecting blood from mice by cardiac puncture into a heparin-containing tube, collecting the supernatant immediately after centrifugation, freezing it at 80C and transporting it at low temperature to a testing contractor (Nikken Seil, Tokyo, Japan). The limit of detection for insulin levels was <0.1ng/mL.

While the mice were 510weeks old, hind paw withdrawal response to thermal stimuli of radiant heat was measured using a Plantar test (Catalog No. 57820; Ugo Basile, Comerio, Italy)47,48. The PWL at 5weeks of age was measured a few days before STZ and the buffer administration. We adjusted the two kinds of IR intensities to a PWL baseline of about 7s (IR=40) and 12s (IR=20). After 30min acclimation, paw withdrawal latencies (PWL) were measured 68 times per session, separated by a minimum interval of 5min. Paw withdrawals due to locomotion or weight shifting were not counted. Data are expressed as paw withdrawal latency in seconds.

Mice were killed after anesthesia with isoflurane, and dorsal root ganglia (DRG) were quickly harvested and placed on ice. The tissue was then immediately immersed in RNAlater Stabilization Solution (Invitrogen). After temporarily storing at 4C, RNAlater was removed, and an appropriate volume of Isogen II (Nippon Gene, Tokyo, Japan) was added to homogenize the ganglia with a Biomasher II apparatus (Nippi, Tokyo, Japan); they were completely homogenized and cells were lysed on ice. Then, total RNA was collected using Ethachinmate (Nippon Gene, Tokyo, Japan) and 75% isopropanol and RNA concentration was assayed using a NanoDrop One Microvolume UVVis Spectrophotometer (Thermo Fisher Scientific, United States). The RNA was reverse transcribed into cDNAs with ReverTra Ace qPCR Master Mix (Toyobo, Osaka, Japan) according to the manufacturers protocol. TRPV1, TRPA1, and 36B4 mRNA levels were assayed using a StepOnePlus Real-Time PCR System (Applied Biosystems) with SYBR Green Real Time PCR Master Mix Plus (Toyobo, Osaka, Japan) according to the manufacturers protocol. All data were analyzed using StepOne software (version 2.3; Life technologies).

The primer sequences used for qRT-PCR were as follows: TRPV1 (NM_001001445), 5-CCCGGAAGACAGATAGCCTGA -3 (forward) and 5-TTCAATGGCAATGTGTAATGCTG-3 (reverse); TRPA1 (NM_177781), 5-GTCCAGGGCGTTGTCTATCGG -3 (forward) and 5-CGTGATGCAGAGGACAGAGAT-3 (reverse); 36B4 (NM_007475.5), 5-AGATTCGGGATATGCTGTTGGC-3 (forward) and 5-TCGGGTCCTAGACCAGTGTTC-3 (reverse).

DRG were isolated and rinsed immediately in ice-cold phosphate-buffered saline (PBS; calcium- and magnesium-free) and put into an appropriate amount of protein lysis buffer (25mM TrisHCl [pH 7.6], 150mM NaCl, 0.1% sodium dodecyl sulfate [SDS], 1% Nonidet P-40, and 1% protease inhibitor), and homogenized using a Biomasher II apparatus. The homogenates were then placed on ice for 30min to ensure complete lysis. Subsequently, the homogenates were centrifuged at 15,000 g for 30 min at 4 C and the supernatant was transferred to a new centrifuge tube. After measuring the protein concentration of each sample using a BCA Assay Kit (catalog No. 297-73101, Fujifilm Wako Chemicals), equal amounts of protein from the DRG were denatured at 95 C for 5 min and electrophoresed on 4%12% SDSpolyacrylamide gel. The proteins were transferred onto a poly(vinylidene fluoride) membrane. Nonspecific binding sites on the membranes were blocked using Tris-buffered saline (TBS) supplemented with 0.05% Tween 20 (Takara Bio, Shiga, Japan) (TBS-T) and bovine serum albumin (BSA) for 1 h at room temperature (RT), and incubated overnight at 4 C with rabbit anti-TRPV1 antibody (13000, Dr. Kido, Saga Medical School Faculty of Medicine, Saga University) and rabbit anti--actin antibody (13000, Cell Signaling Technology). Then anti-rabbit IgG HRP-linked secondary antibodies (11000, Cell Signaling Technology) were incubated with the membranes for 1 h at RT. Between respective steps, the immunoblots were rinsed with TBS-T 3 times for 10 min each time. All protein bands were labeled using an ECL kit (Amersham, United Kingdom) and then visualized using an ImageQuant LAS 4000 system (General Electric). The densities were normalized with respect to the -actin level.

According to a published method49 with some minor modifications described as follows, DRG were isolated from 5 to 10week old mice. In brief, resected DRG were collected in PBS (calcium- and magnesium-free) on ice, and then the tissues were incubated with 725g of collagenase type IX (catalog No. C9407, Sigma-Aldrich) in 250 L of Earles balanced salt solution (Sigma-Aldrich) containing 10% fetal bovine serum, MEM vitamin solution (1:100, Sigma-Aldrich), penicillinstreptomycin (1:200, Life Technologies), and GlutaMax (1:100, Life Technologies) at 37C for 30min. Next, the DRG neurons were dissociated by triturating the suspension through a fire-polished Pasteur pipette and filtering it through a 70m cell strainer (Flowmi). The isolated neurons were placed on 12mm diameter coverslips (Matsunami, Osaka, Japan) with 20 L of Earles balanced salt solution and used for experiments within 2h of isolation, maintaining them at 37C in a chamber under a humidified atmosphere of 95% O2 and 5% CO2.

Ca2+ transients were measured in isolated cultured DRG neurons incubated with 5mM Fluo-2-AM (Molecular Probes, Invitrogen) for 20min at 37C, and DRG were mounted in an open chamber and superfused with bath solution. The extracellular standard bath solution contained 140mM NaCl, 5mM KCl, 2mM MgCl2, 2mM CaCl2, 10mM HEPES, and 10mM glucose at pH 7.4, adjusted with NaOH. Cytosolic free Ca2+ concentrations were measured by dual-wavelength Fura-2 microfluorometry with excitation at 340/380nm and emission at 510nm. Fura-2 fluorescence was recorded with a CCD camera, CoolSnap ES (Roper Scientific/Photometrics). Data were acquired using imaging processing software IPlab (Solution Systems, Funabashi, Japan) and analyzed with ImageJ 1.53 (NIH). At the end of each experiment, ionomycin (5M) was applied in the presence of 20mM extracellular CaCl2 to obtain saturating levels of Ca2+ influx as Fmax. The population that did not respond to either molecular stimulus, responded to AITC alone, capsaicin alone, and the population responding to both stimuli were determined by the number of neurons responding to capsaicin and/or AITC divided by the number of neurons responding to ionomycin and expressed as a percentage.

Distal sciatic nerve tissue was prepared for imaging as previously described with slight modifications50. WT (non-DM), WT (DM) and TRPV1/ (non-DM) mice (5weeks after STZ administration or the same age) were perfused with 2.5% glutaraldehyde and 4% paraformaldehyde in 0.1M phosphate buffer. We collected sciatic nerves from the same position for all mice, and these tissues were post-fixed for 4h, and maintained at 4C overnight. The samples were post-fixed in cold 2% OsO4 in PBS for 60min, dehydrated in a graded ethanol series and acetone and embedded in Quetol 812 epoxy resin (Nisshin EM Co.). The resin was incubated at 70C for 3 nights to ensure polymerization. Prior to TEM observation, semithin, 1m-thick sections were cut and stained with 1% toluidine blue for examination by light microscopy (AX80; Olympus). Ultrathin sections(70nm-thick) were prepared with an ultramicrotome (ULTRACUT S, Reichert-Nissei) and stained with uranyl acetate and lead citrate. The ultrathin sections were observed by TEM (HT7700; Hitachi High-Tech). Image analysis was performed with Image J software. The g-ratios were calculated by dividing the axon diameter by the diameter of the axon including the myelin. The diameter was calculated by the measured perimeter divided by .

The Thermal Gradient Ring (Catalog No. 35550; Ugo Basile) is an apparatus with 45cm inner diameter, 57cm outer diameter, and 24cm height. A camera is located on the upper side of the apparatus, which includes an infrared camera and an infrared transmissive inner wall. The cooling and heating devices were set so that the surface temperature range of the apparatus was from 10 to 55C. Floor surface temperature was monitored using a thermometer (HFT-51, Anritsu, Japan). Behavioral assays were performed between 9:00 and 17:00. All mice were acclimated for 30min in the thermal gradient apparatus with its floor at room temperature (2324C) before the day of the thermal gradient test. Mice were placed individually in the device in an innocuous mid-temperature zone. The behavioral data was videotaped for 60min and analyzed as spent time, travel distance or speed automatically using ANY-maze software. We defined preference temperature as the mean value using the zone temperature and spent time.

Data are presented as meansSEM. Statistical analysis was conducted using GraphPad Prism 9.2.0 (GraphPad Software, United State). Significant changes were identified using a two-tailed t test, at 95% confidence interval, or one-way ANOVA and two-way repeated measures ANOVA followed by a Bonferroni post hoc test with p<0.05 considered as significant (p: *<0.05, **<0.01, ***<0.01).

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Thermal gradient ring reveals thermosensory changes in diabetic peripheral neuropathy in mice | Scientific Reports - Nature.com

PARIS--(BUSINESS WIRE)--Regulatory News:

GenSight Biologics (Paris:SIGHT) (Euronext: SIGHT, ISIN: FR0013183985, PEA-PME eligible), a biopharma Company focused on developing and commercializing innovative gene therapies for retinal neurodegenerative diseases and central nervous system disorders, today announced that it will participate to the EUNOS 2022 meeting, which is taking place on June 20-23 in Birmingham, United Kingdom. The conference is the most important conference in Europe for neuro-ophthalmologists and provides GenSight the opportunity to discuss its clinical data and recent developments with the neuro-ophthalmology community. The Company is a sponsor of EUNOS and will have a booth on site.

Patrick Yu-Wai-Man, MD, PhD, Professor of Ophthalmology and Honorary Consultant Neuro-ophthalmologist at the University of Cambridge, Moorfields Eye Hospital, and the UCL Institute of Ophthalmology, United Kingdom, will present on two topics relevant to Leber Hereditary Optic Neuropathy (LHON). He will first present data from GenSights Phase III REFLECT trial and discuss the efficacy of the Companys bilateral treatment approach. He will also discuss the future of LHON treatment.

The long-term follow-up data of patients in the REFLECT trial illustrate the sustained effect of the treatment and the clear impact on visual acuity for patients affected with LHON, he said. The data will be of particular interest to physicians seeking an effective treatment for this blinding mitochondrial disorder.

15th annual meeting of EUNOS (European Neuro-Ophthalmological Society) - EUNOS 2022

June 20-23, 2022 - University of Birmingham, Edgbaston, Birmingham, UK

The Phase III REFLECT trial: efficacy of bilateral gene therapy for Leber Hereditary Optic Neuropathy (LHON) is maintained 2 years post administration, presented by Patrick Yu-Wai-Man, MD, PhD, University of Cambridge, United Kingdom (principal investigator in the RESCUE, REVERSE, RESTORE, REFLECT and REALITY trials; international coordinator of the REVERSE trial).

Future Treatment for Lebers hereditary optic neuropathy, presented by Patrick Yu-Wai-Man, MD, PhD, University of Cambridge, United Kingdom (principal investigator in the RESCUE, REVERSE, RESTORE, REFLECT and REALITY trials; international coordinator of the REVERSE trial).

GenSight Biologics will also lead a presentation on GS010 (Lenadogene nolparvovec) clinical data at the Global 7th Cell & Gene Therapy Summit, July 19-21. Magali TAIEL, MD, Chief Medical Officer of GenSight Biologics, will make a presentation titled, Development of GS010 gene therapy in Leber Hereditary Optic Neuropathy: Key learnings.

About GenSight Biologics

GenSight Biologics S.A. is a clinical-stage biopharma company focused on developing and commercializing innovative gene therapies for retinal neurodegenerative diseases and central nervous system disorders. GenSight Biologics pipeline leverages two core technology platforms, the Mitochondrial Targeting Sequence (MTS) and optogenetics, to help preserve or restore vision in patients suffering from blinding retinal diseases. GenSight Biologics lead product candidate, LUMEVOQ (GS010; lenadogene nolparvovec), has been submitted for marketing approval in Europe for the treatment of Leber Hereditary Optic Neuropathy (LHON), a rare mitochondrial disease affecting primarily teens and young adults that leads to irreversible blindness. Using its gene therapy-based approach, GenSight Biologics product candidates are designed to be administered in a single treatment to each eye by intravitreal injection to offer patients a sustainable functional visual recovery.

Originally posted here:
GenSight Biologics Announces Participation and Presentation of GS010 Clinical Data at EUNOS 2022 - Business Wire

I'm the Chief Medical Officer of WebMD and also a practicing physician. I have a keen interest in getting people better information so they can have better health. Diabetes is one of those areas where there are so many myths. Sadly, misinformation can lead to poor health. More than 34 million Americans have diabetes that's nearly 1 out of every 10 people. Over 1.5 million people are diagnosed every single year. Another 88 million people have prediabetes. And the numbers are going up. As a nation and as individuals, we need to get our blood sugar under control. The first step is getting good information about the signs and symptoms of diabetes. Read on to find out moreand to ensure your health and the health of others, don't miss these Sure Signs You've Already Had COVID.

There are different signs and different people present with different symptoms. In general one of the first signs is polyuria a fancy word that basically means you start to pee a lot. What's a lot? Most people urinate 8-10 times a day; if you are going to the bathroom 12 or more times a day, it's time to get checked. The high sugar in your blood is also making sugar go into your urine and that's pulling water out of your cells. Therefore, you urinate much more frequently.

Because of the increased urination, you typically become more thirsty. You tend to be thirsty all the time, even after you drink. It's a thirst that lasts throughout the day, even after night. You just can't seem to quench your thirst. I will always remember my patient, Mary, who knew something was wrong. "Dr. Whyte, I was drinking water constantly and I don't even like water. When I drank from the sink one day, I knew I had to come in!"

Although most people gain weight when they have diabetes, and they have more food cravings, some people actually lose weight early on with untreated and undiagnosed diabetes. Insulin resistance prevents the body from getting glucose from the blood into the body's cells to use as energy. When this occurs, the body starts burning fat and muscle for energy, causing a loss in body weight. Your body also dumps a lot of sugar in the urine, reducing your number of calories. This is not a healthy weight loss.6254a4d1642c605c54bf1cab17d50f1e

Numbness and tingling often result after several years of diabetes. But because people often don't know the signs and symptoms, some present with tingling in their hands and feet. It's called "diabetic neuropathy" and is nerve damage caused by chronically high blood sugar. It leads to numbness, loss of sensation, and sometimes pain in your feet, legs, or hands. The bad news is that once you develop diabetic neuropathy, it can be very hard to treat. Medications often treat symptoms but don't reverse the damage. The key is to prevent it from developing.

Sometimes people complain of fatigue. They are tired all the time. It's not a feeling that is just a few days but rather goes on for months. People often think they are working too hard or just out of shape. Fatigue can be the result of several health conditions but if you are more tired than usual, it is a good idea to get checked for diabetes since high blood sugar from insulin resistance prevents you from getting the energy your cells need.

If you experience any of these symptoms, you should immediately go to the doctor and get a lab test. There are numerous tests, and you don't always have to be fasting. The doctor may do a random plasma glucose and a glycosylated hemoglobin. Based on those results, your doctor will decide with you the best next steps. The American Diabetes Association (ADA) recommends that everyone over the age of 45 be screened for pre-diabetes and diabetes. In addition, the ADA also recommends adults at any age get screened who are overweight or has one or more risk factors.

Diabetes is a serious disease. It's the number one cause of blindness in the US and a leading cause of kidney disease. It increases one's risk of heart disease and stroke dramatically. The encouraging news is there are numerous options to treat it including lifestyle changes and drugs. For many people, if they change the way they eat, exercise, and deal with stress, and act early, they may be able to reverse Type 2 diabetes or at least prevent its complications. And to protect your life and the lives of others, don't visit any of these 35 Places You're Most Likely to Catch COVID.

Dr. John Whyte CMO of WebMD is an expert on preventative care and author of the Take Control Series.

John Whyte, MD, MPH

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Warning Signs of Diabetes, Says Physician Eat This Not That - Eat This, Not That

During (National) Diabetes Awareness Week from 13 to 19 June 2022, Neuropad a 10-minute pain-free screening test for the early detection of diabetic foot syndrome, a condition which can lead to serious complications such as foot ulceration, and amputation is raising awareness about this condition. Foot complications are the most feared of all the complications of diabetes, however, alarmingly, 30% of people with diabetes are unaware that foot complications are common and serious if detected late. Another sobering statistic is that the five-year mortality post amputation is worse than most common cancers and much higher than breast cancer.

Nerve damage to the feet is a common complication of diabetes, but often goes unnoticed. Neuropad helps solve this problem with a simple colour change test, that provides an early warning sign.

Neuropad believes in prevention is better than the cure and is supported by the Paula Carr Diabetes Trust and has also recently been recommended by the National Advisory Panel for Care Home Diabetes (NAPCHD) in its new national guidance for care home operators and their staff. Neuropad doesnt need a healthcare professional to apply the test and people can easily do the test at home unaided.

The NAPCHD new national guidance, has been created by an eminent panel of UK healthcare professionals led by Professor Alan Sinclair FRCP. The panel included Professor Gerry Rayman FRCP, MBE, a well-known and respected expert in diabetic foot disease and pioneer of the Touch the Toes Test (TTT) for the detection of sensory neuropathy, which is a complementary test to Neuropad. The new guidance recommends care home staff to screen residents with diabetes at risk of developing peripheral neuropathy with Neuropad in conjunction with the TTT. Half of all people with diabetes may develop peripheral neuropathy, including peripheral autonomic neuropathy. Often complications develop before treatment starts and early identification of possible problems is an advantage, allowing interventions to start early.

UK government data - published by the Office for Health Improvement and Disparities - looked at the three years leading up to the pandemic. It found 13 out of 135 local areas in England had significantly higher rates of foot amputations. It is believed up to 80% of foot amputations could be avoided with better care.

The charity Diabetes UK has stated that these figures were incredibly concerning and the figures "shined a light on the scale of the crisis facing diabetes care." It warned access to support was likely to have become worse during the pandemic. A recent report by the charity said lives would be needlessly lost because of disruption to services over the past two years.

80,000 people in England have a foot ulcer each year and 8,000 lose a limb because of diabetes. These types of amputations are a sign patients have not received adequate care, as poorly controlled diabetes increases the risk of foot ulcers and infections. It costs NHS England 1.1 billion in direct medical costs alone. Neuropad believes it is a ticking time bomb, which gets worse each year by between 15% and 20%.

The Paula Carr Diabetes Trust is an independent charitable trust supporting people in Kent & Medway living with diabetes. It has been using Neuropad in its centres, where diabetes specialists provide integrated care, treatment, screening, and health education for people living with diabetes in their areas.

Gary Fagg, MBE, Chairman of Trustees at the Paula Carr Diabetes Trust says, If you have diabetes your feet need special attention, because diabetes can reduce the supply of blood to your feet and cause a loss of feeling. People may not notice that they have lost the feeling in their feet so there is risk that a minor injury could develop into serious complications, including amputation due to gangrene. This is where Neuropad comes in, a simple pain-free patch test for the feet, will help people avoid and detect any problems early on. The COVID-19 pandemic has affected people being seen in time by the NHS and at the Trust we are seeing a rise in unnecessary amputations. This is another pandemic! We fully support Neuropad, a test that people can do at home.

Gary Fagg, MBE, is happy to talk about how he lost his younger brother who died of diabetes, who had lost his leg to this disease.

Prof. Sinclair, Internationally and Nationally Recognised In The Field Of Diabetes In Older People, World Health Organization-recognised Expert In Diabetes says, Neuropad offers the opportunity to test for the early signs of distal neuropathy which is an important risk factor for diabetic foot disease. In people with diabetes who because of moderate to severe frailty, dementia, or sensory deficits affecting the eyes or hearing, the Neuropad test provides an assessment of nerve function that does not require verbal input from the individual being examined. As such, it can be seen as a complimentary test to other more established tests of neuropathy.

John Simpson, CEO Neuropad says, Look at these dreadful statistics - 80,000 people in England have a foot ulcer each year and 8,000 lose a limb because of diabetes! Neuropad has the potential to be a real game-changer, as the early detection of foot ulcers will allow treatment to start quickly and consequently will have the potential to have positive economic benefits too. The Neuropad test will go towards helping to provide the highest possible standards of diabetes care and level the playing field in terms of health inequality as it is so easy to use.

How Neuropad Works

Damage to the nerves in the feet because of diabetes can result in the sweat glands not producing enough moisture, leading to dry and cracked feet. The medical term for this is sudomotor dysfunction. Neuropad which has undergone rigorous academic research, is stuck to the sole of each foot like a sticking plaster and left in place for 10 minutes. The pad is blue to start with and should turn pink, in the presence of moisture from sweating, to indicate a normal result. If the Neuropad test patch stays blue, or if it turns a patchy blue/pink, then this indicates that you may have some level of nerve damage and that your sweat glands are not working properly as there is not enough moisture to complete the colour change. Colour blindness may make it difficult to distinguish blue from pink. If that is the case, then ask for help to check the results.

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Foot Disease: The Most Feared Of All The Consequences Of Diabetes - Pressat

Many cancer survivors may think the stress and anxiety are cured along with the disease, but that is not always the case. Stress, anxiety and pain can remain after cancer treatment has ended but practicing daily meditation may help.

Meditation is a mind-body complementary therapy that research has shown improves mood and sleep, in addition to helping with anxiety and pain. These are side effects that cancer survivors commonly encounter as a result of their disease and treatment. So how can meditation help and how to start?

Erin OCarroll Bantum, a clinical health psychologist at the University of Hawaii Cancer Center spoke with Heal, a sister publication of CURE, about meditation.

What is meditation and how can it help?

There are many different types of meditation, Bantum explained, but she primarily focuses on mindfulness meditation for cancer survivors.

Mindfulness meditation allows someone to notice their racing thoughts and sensations in their body, and oftentimes, in simply noticing, the body and mind can calm. Bantum described mindfulness meditation as paying attention to what is, noticing experiences and being with them but not attaching to them.

As previously mentioned, research has demonstrated that mindfulness mediation can improve things such as pain, how pain is perceived, anxiety and stress. And current research is evaluating if it also can improve neuropathy a common side effect in cancer survivors.

I like to think of it as more of an umbrella intervention, she explained. There are going to be specific side or late effects that we will want to impact (with meditation) that are bothersome to people. But the general practice is to really look at our overall experience. As we do that and extend that into our everyday life, it becomes relevant in interactions with others (and) it can improve our function and social interactions.

Bantum added that many cancer survivors who come to her looking for a new approach to ease what they are going through often feel isolated. They may feel lost after treatment is over and that others dont understand what they are going through. Meditation has been shown to improve mood, so this might be helpful for cancer survivors who are feeling this way, Bantum explained.

I think building those habits in general such as mindfulness meditation having those things we can consistently do for our physical and mental health, I think that stability is really grounding when the experience of cancer can be so ungrounding, she said.

Tips for meditating

Bantum noted that it is important to make a commitment to meditation she said the best way to reap the benefits is to practice every day. It is not a long process, she said. A good start would be five to 10 minutes then working up to 20 minutes of mindfulness meditation, either first thing in the morning or right before bed.

I think sometimes if we expect something unreasonable, in terms of how much time we actually have to devote, we can feel overwhelmed and then we might not practice at all, she added. Try to suspend any judgment about the experience for a while. Give yourself a few weeks if you can, and even if it feels like its going nowhere, see how it really feels to continue the practice. The best way to know what to keep including in your life is to really feel it out yourself, especially if you can sit through some natural discomfort to see whats underneath.

A step-by-step guide to start meditating

Bantum explained that meditation can be overwhelming at first. When sitting down and trying not to think of anything, often everything then comes to mind. But if a cancer survivor would like to try meditation, she recommends following these steps:

For more news on cancer updates, research and education, dont forget tosubscribe to CUREs newsletters here.

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How Mindfulness Meditation May Help Ease Stress and Anxiety in Cancer Survivors, and Where to Start - Curetoday.com

When you are looking to find the best strain to treat your pain, you need to be sure to look into the different types of cannabis strains and their effects. While it is common for a strain to be effective for treating certain types of pain, this is not always the case. Some companies produce strains that have different effects. It is important to research the different properties of different strains to find the best one and buy marijuana seeds only at at a trusted source if you want to grow them at home

The main terpenes of a strain vary, as can the CBD/THC ratio. Other cannabinoids such as CBG and CBN are present in some strains. Because everyones physiology and experience with cannabis is different, you will need to experiment with several strains before finding one that works for you.

If you are looking for a potent pain reliever, consider an Indica strain. This strain is known for its sedative and calming effects, and it is also very popular with nighttime smokers. Its high concentrations of terpenes make it effective for relieving pain and inflammation, but it also makes the user sleepy. Typically, you should save this strain for nighttime use.

The most popular and effective indica strain for pain treatment is Northern Lights. This strain is so powerful that it completely relaxes the body without giving the user a psychoactive high. It can relieve neuropathic pain and is easily available at most medical marijuana dispensaries. It also works well for neuropathic pain, as its body high will relieve all the tension. However, it is important to note that neuropathic pain is not the only type of chronic pain that can be relieved by cannabis.

An indica plant is native to the mountainous regions of the world, and was adapted to cold climates by incorporating many characteristics of its natural habitat. Its shorter squat structure makes it an ideal candidate for pain relief. It produces dense buds and flowers, and is also known for its sedative and body-oriented effects. This plant is also popular with those who suffer from muscle spasms and insomnia.

The effects of cannabis vary widely depending on the type of terpenes present in the plant. Those with the highest levels of terpenes, known as cannabinoids, are known for their euphoric effects. In addition, terpenes are known to enhance the effects of major cannabinoids, such as THC. The majority of cannabis contains terpenes, and a large number of terpenes help them to function in the body.

Choosing the right sativa or indica strain for your specific pain is a matter of trial and error. Luckily, most dispensaries offer knowledgeable staff who can help you choose the right strain. It is essential to take a look at the product label to determine what type of strain will work best for your particular pain. This way, you will be sure to select the best one for you.

The Jack Herer marijuana strain is a popular medical strain used to treat chronic pain, depression, and anxiety. Known for its high THC content, Jack Herer is often used to treat various ailment conditions, including migraines and chronic pain. This strain is also effective for treating PTSD and ADHD. The high THC content of Jack Herer can help relieve symptoms of chronic pain and relieve inflammation.

The Jack Herer cannabis strain was developed in the Netherlands in the mid-1990s. Dutch pharmacies distributed this strain as a medical-grade strain. The pine-scented, spicy cannabis plant has won numerous awards. Many breeders have attempted to grow Jack Herer in Mediterranean or sunny climates. Indoor growers should allow 50 to 70 days for flowering. This strain is often recommended for patients with back pain, arthritis, and other chronic pain.

The benefits of the Afghani strain are diverse and range from sedative to physical. The strain is a convenient alternative to pharmaceutical painkillers, reducing the need for sleep. The high THC content in the Afghani strain is a potent pain reliever and helps reduce nausea and anxiety. Many people find this strain to be a calming alternative to prescribed medication. This cannabis strain is also known for its sedative effect and is suitable for treating chronic pain, anxiety, and insomnia. Its euphoric effects and ability to cure pain can also be attributed to its calming and meditative properties.

Although the Cannatonic has low levels of THC and sedative effects, its uplifting effects make it a good choice for chronic pain and neuropathy. Its uplifting effects help combat the negative emotions caused by chronic pain. Another good choice for treating pain is the Jack Herer, a mild sativa strain with an average THC content of 18-24%. Jack Herer has an uplifting cerebral and physical high. Its a good choice for new cannabis users who are concerned about their health or the type of pain they suffer.

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TYPES OF CANNABIS STRAINS AND THE TYPE OF PAIN THEY TREAT - GISuser.com

There are various types of neuropathy depending on what nerves are damaged, compressed or defective. Peripheral neuropathy is the most common, but there is also proximal, cranial, autonomic and focal neuropathy. Your symptoms can stem from one nerve being affected (mononeuropathy), all your nerves (poly) or two nerves being damaged (multiple mononeuropathy). Learn about the various types of neuropathy, how they affect you and how you can treat them at Spine Correction Center of the Rockies.

An estimated 20 million people in the United States have some form of neuropathy. As we mentioned, there are five main categories to consider. Common types of neuropathyare broken down for you below:

Peripheral Neuropathy is the most common form of neuropathy in patients. This condition results from damage to the peripheral nervous system the massive communications network that manages information between the central nervous system (the brain and spinal cord) to every other part of your body. This particular nerve damage affects areas such as your toes, feet, legs, fingers, hands and arms. Many patients find that complementary and alternative therapies are effective in managing pain caused by peripheral neuropathy.

Proximal Neuropathy is the second most common form of neuropathy. This form of neuropathy encompasses nerve damage in your thighs, hips or gluteal areas of your body. The condition usually affects one side of the body, but can spread to the other side as well.

Cranial Neuropathy is a condition describing nerve damage to any of the 12 cranial nerves. The cranial nerves are those that travel from your brain or brainstem. These nerves affect areas like the face and eyes. Johns Hopkins medical library breaks down the the different types of cranial neuropathies as:

Autonomic Neuropathy occurs when nerves of your involuntary nervous system (the heart, circulation, digestion, sweat glands, bowel and/or bladder, and sexual organs) are damaged. While diabetes is the most common cause of autonomic neuropathy, other health conditions or infections can also trigger autonomic neuropathy symptoms. Some medications have been shown to cause this particular kind of nerve damage as well.

One of the less common forms of neuropathy, Focal Neuropathy, sometimes referred to as mononeuropathy, affects a single nervecommonly, those of the wrist, thigh, or foot, although it can sometimes affect the nerves of the back and chest, as well as those that control the eye muscles. Diabetes is often the root cause of this form of neuropathy.

When it comes to identifying the cause of your neuropathy symptoms, a thorough evaluation is essential. Neuropathy may be caused by:

To diagnose your particular symptoms, and to get to the root of your problem, involve a specialist at Spine Correction Center of the Rockies. Not only can a specialist uncover the cause of your symptoms, but they can also prescribe targeted treatment options to restore function and eliminate pain.

Dont be tempted to mask your symptoms with narcotics or over-the-counter medications. The only correct way to treat neuropathy is to identify the underlying cause and address the abnormality. Controlling blood sugar levels, treating alcohol abuse, improving ones nutrition, treating or managing autoimmune diseases, correcting the spinal, muscle or bone structural abnormalities through non-invasive, chiropractic therapies are some of the solid treatment strategies that need to be implemented in individual cases depending on the cause of neuropathy.

If you are a victim of the pain and dysfunction neuropathy can cause, dont postpone getting help from a specialist in the field! Spine Correction Center of the Rockies offers you expertly-trained chiropractors and medical personnel, prepared to diagnose the cause of your neuropathy and plan individual treatment strategy for your needs. We offer non-invasive, drug-free therapies, correction of the underlying medical problem and professional nutritional and lifestyle advice. Call now for a FREE Consultation, (970) 658-5115.

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5 Types of Neuropathy and What to Do About Them | Fort ...

Clival chordoma (CC) is a rare neoplasm that arises from remnants of the embryonic notochord. Common sites of chordoma development are the sacrococcygeal area and the skull base. Intracranial chordomas usually arise from the region of the clivus. Diplopia is a common complaint but isolated optic nerve compression is rare; among intracranial neoplasms, chordomas were found in less than 0.7% of cases. We describe a case of visual loss due to unilateral compressive optic neuropathy as the presenting manifestation of this uncommon intracranial tumor.

A 26-year-old man presented complaining of progressive visual loss in the right eye (OD) for the past eight months. He denied headache, diplopia, or any other neurologic symptoms and felt otherwise well. His past medical history was non-contributory and he was taking no medications. Best-corrected visual acuity (BCVA) was 20/200 OD and 20/20 in the left eye (OS). Extraocular motility was full. External exam was normal and there was no proptosis or ptosis. Pupils were isocoric with a right relative afferent pupillary defect (RAPD). Intraocular pressure measurements and anterior segment examination were within normal limits in both eyes (OU). Fundus examination (Figure 1) revealed optic nerve pallor OD and a normal optic disc OS.

The standard computerized visual field (Figure 2) showed a diffuse defect OD and a superior mild fascicular defect OS. Magnetic resonance imaging (MRI) of the brain showed a large intracranial mass with radiologic features of CC (Figure 3), with the upward displacement of the chiasm and asymmetric involvement of optic nerves (figure 4). The patient underwent subtotal neurosurgical resection and pathology was consistent with a chordoma (Figure 5) but there was no improvement in visual acuity or visual field.

CC is a rare neoplasm with an incidence rate of less than 0.1 per 100.000 per year [1]. CCs arise from remnants of the embryonic notochord [2] and show both epithelial and mesenchymal differentiation. Common sites of chordoma development are the sacrococcygeal area in 50-60% of cases and the skull base (spheno-occipital area) in 25-35% of the cases. Uncommonly, it may develop from cervical, thoracic, or lumbar vertebrae [3].

Histologically chordomas show a typical pattern of lobules separated by fibrous bands. Each lobule displays vacuolated, atypical neoplastic cells within a myxoid stroma [4]. Age at presentation is around the fifth or sixth decades for the sacrococcygeal type and even earlier for skull-base chordomas [3].

In several large reviews of patients with intracranial neoplasms, chordomas were found in 0.1-0.7% of patients [5]. Intracranial chordomas usually arise from the region of the clivus and account, as previously reported, for about one-third of all cases [3]. Although the tumor rarely metastasizes, advanced secondary lesions may affect the lungs, bone, liver soft tissues, lymph nodes, and skin [6].When arising from the clivus, common symptoms are headache, facial numbness, nasal discharge, dysphagia, and cranial nerve palsy. Diplopia is a common complaint since the most common cranial nerve to be compressed is the sixth cranial nerve with unilateral or bilateral abducens deficit. Third and fourth nerve palsies are also possible as well as complete unilateral ophthalmoplegia from multiple cranial nerve involvement.

Volpe and coworkersreviewed the neuro-ophthalmologic findings in chordomas and chondrosarcomas of the skull base [5]. In the group of 48 patients with chordoma, decreased visual acuity was present in only four patients (8%) but in only two cases (4%) was visual loss an isolated finding.The pattern of the visual field loss differed in each patient, with some displaying a central scotoma, altitudinal defects, junctional scotoma, or bi-temporal hemianopsia. In a series of 12 patients, Harbour and coworkers found that visual loss was present in only three patients (25%), but none of them complained of visual loss as the presenting symptom [7]. In another case series of 63 patients affected by intracranial chordoma, Bagan et al. found 39 patients (62%) with isolated ophthalmic manifestations [8].Visual loss was present in only 10 patients (16%) and among those patients who initially had only one symptom, only three of them (4.7%) complained of isolated visual loss.

Although isolated and progressive unilateral visual loss from compression of the anterior visual pathway is an uncommon finding in CC, clinicians should be aware of this presentation. Neuroimaging typically demonstrates the compressive lesion and the origin at the clivus consistent with CC. Gross total resection is the best treatment.

Read more here:
Unilateral Compressive Optic Neuropathy As the Presenting Manifestation of Clival Chordoma: A Case Report - Cureus

Trigeminal neuropathies (TNp) are a group of well-characterized disorders that involve damage to or infiltration of the trigeminal nerve. The underlying etiology of trigeminal neuropathy can be traumatic, inflammatory, autoimmune, paraneoplastic, malignant, and very rarely infectious. We present a case of trigeminal neuropathy due to local malignant invasion of the mandibular nerve with mandibular nerve enhancement at the foramen ovale and foramen rotundum. In the process, we review various etiologies of trigeminal neuropathy associated with trigeminal nerve involvement at the foramina. We emphasize the importance of a comprehensive evaluation in patients with trigeminal neuropathy, which includes searching for perineural spread or invasion by a local head and neck malignancy, as well as ruling out an inflammatory or autoimmune etiology. Our case also demonstrates that a higher field strength magnet can reveal pathology unseen with a lower field strength magnet.

The trigeminal nerve, cranial nerve V, is the largest of the 12 cranial nerves and has mixed sensory and motor functions. Its origin is in the brainstem and includes three sensory nuclei (mesencephalic, principal sensory, and spinal nucleus of the trigeminal nerve) and one motor nucleus (motor nucleus of the trigeminal nerve). Sensory information travels via afferent neurons from the face to the trigeminal ganglion and distributes via the various sensory trigeminal nuclei. Sensory information, such as pain and temperature, is then relayed to the contralateral thalamus and eventually synapses in the postcentral gyrus. Motor information travels via efferent neurons from the motor nucleus directly to its targets: masseters, temporalis, and pterygoid muscles [1,2].

The trigeminal nerve divides into three branches at the Gasserian ganglion in Meckels cave [3]. The three branches consist of the ophthalmic nerve (V1), the maxillary nerve (V2), and the mandibular nerve (V3). The ophthalmic nerve (V1) travels through the cavernous sinus, exits the base of the skull, and enters the orbit via the superior orbital fissure. The maxillary nerve (V2) accompanies the ophthalmic nerve in the cavernous sinus as it makes its way to the pterygopalatine fossa by exiting the skull base via the foramen rotundum. At the pterygopalatine fossa, the maxillary nerve splits into many branches. A trigeminal nerve deficit (V1 and V2) and a sixth nerve palsy localize a lesion to the cavernous sinus. The mandibular nerve (V3) does not traverse the cavernous sinus but runs along and eventually exits the base of the skull via the foramen ovale into the masticator space [4].

The ophthalmic and maxillary nerves are sensory branches of the trigeminal nerve. The ophthalmic division branches into the frontal, lacrimal, nasociliary, tentorial, and dural nerves. These nerves provide sensory innervation to the cutaneous surfaces of the upper eyelids, forehead, and sides of the nose. The nasociliary nerve specifically innervates the tip and the sides of the nose, and its involvement in herpes zoster ophthalmicus is known as Hutchinsons sign. The ophthalmic branches also innervate the mucosa of the frontal sinus, lacrimal glands, cornea, conjunctiva, ciliary body, and dura mater [5]. Damage to some of these branches, more specifically to the parasympathetic efferent nerves of the lacrimal glands, can manifest as dry eyes in Sjogrens syndrome. The maxillary division of the trigeminal nerve branches into the infraorbital, zygomatic, greater palatine, lesser palatine, posterior superior alveolar, and meningeal nerves. These nerves provide sensory innervation to the region below the orbit and above the mouth, the maxillary teeth, and the maxillary sinus.

The mandibular division of the trigeminal nerve is unique in that it branches into both sensory and motor nerves. Sensory nerves include meningeal, lingual, auriculotemporal, inferior alveolar, buccal, and mental nerves. A mental neuropathy with numbness of the chin is a sinister sign of local malignant invasion. These nerves provide sensory information to the region below the mouth, the mandibular teeth, and the anterior two-thirds of the tongue. The motor nerves include the masseteric, deep temporal, medial pterygoid, lateral pterygoid, and mylohyoid branches. A motor nerve root supplies the tensor veli palatini, a lesion of which causes palatal myoclonus. Another motor twig goes to the tensor tympani, and injury here leads to hyperacusis [2,5]. It should also be emphasized that the mandibular branches, with the ophthalmic branches, supply the dura mater of the anterior and middle cranial fossa.

Neoplastic, autoimmune, paraneoplastic, and autoimmune processes can damage the trigeminal nerve, leading to trigeminal neuropathy (TNp) [6,7]. The characteristic findings of TNp include facial numbness and weakness of the muscles of mastication. TNp is different from trigeminal neuralgia (TN), which is characterized by episodes of sudden, very brief, severe, sharp, shooting facial pain. The initial presentation of TNp can include pain; however, with disease progression, facial numbness and masticatory muscle weakness may predominate [8]. As TNp may be the initial presentation, malignancies of the head and neck should always be in the differential diagnosis, and a high-resolution magnetic resonance imaging (MRI) of the brain and skull base with and without gadolinium enhancement is paramount [9].

We present the case of a relatively healthy 80-year-old female who presented to the clinic with a several month history of recurrent sharp, shooting left midfacial pain. The pain was associated with tingling in the left half of the face and loss of taste. With initial symptom presentation, the patient went to the emergency department and was diagnosed with Bells palsy and was given gabapentin for the pain. At her follow-up at the neurology clinic, she presented with unimproved symptoms in addition to newly developed left lower facial weakness and occasional chewing difficulty. She denied hyperacusis.Twenty years ago, she had presented with a left midface nodule, which was excised and diagnosed as a basal cell carcinoma. She has not had a recurrence since.

Her past medical history is significant for hypertension, for which she takes lisinopril 10 mg once daily. The patient denied any significant family history. She has never smoked, does not consume alcohol, and denies using any illicit or recreational drugs. Constitutional symptoms including weight loss, fever, and malaise were not reported.

Vital signs revealed a blood pressure (BP) of 170/91 mmHg with a pulse of 81 beats per minute and oxygen saturation of 97%. The patients height was 5 feet and 8 inches with a weight of 185 pounds and a body mass index of 28.1 kg/m2. Physical examination showed a well-nourished individualwhowas alert, relaxed, and cooperative. The patient was oriented to person, place, situation, and time. Gait was steady with a normal base, arm swing, and turning. Heel- and toe-walking was normal with an absent Romberg sign. Speech was of normal tone, volume, and prosody.

Cranial nerve examination revealed normal extraocular motion with symmetric pupils and preserved accommodation, and visual fields were full to confrontation. There was a striking decrease insensationto touch and pinprick over the left V2 and V3 distribution. The corneal reflex was brisk bilaterally. No masseter or temporal muscle atrophy was noted bilaterally. Left lower facial weakness was noted with depressed nasolabial fold, inability to blow the left cheek,andconspicuous sagging of the left lower face. Hearing was intact to finger rub bilaterally. The gag reflex was preserved bilaterally with a tongue that protruded to the midline. The trapezii and sternocleidomastoids were well developed and symmetric, and she executed shoulder shrug and head-turning with adequate power.

Motor examination showed good muscle bulk and tone. No pronator drift or spastic catch of the arms was noted, and the legs were of normal tone. Strength was graded at 5/5 with the Medical Research Council (MRC) rating scale in the upper and lower extremities bilaterally. Sensation to vibration, position, light touch, and pinprick was normal in the fingers and toes. Deep tendon reflexes (biceps, triceps, brachioradialis, patellar, and Achilles) were lively and bilaterally symmetric. Babinski sign was absent bilaterally. Finger-to-nose and heel-to-shin motions were normal bilaterally. An initial 1.5-Tesla MRI of the brain with and without contrast revealed an asymmetrical enhancement of the left mandibular branch of the trigeminal nerve as it extended through the foramen ovale(Figure 1).

A second 3-Tesla high-resolution MRI of the brain and skull base with and without contrast showed far more detail than the lower 1.5-Tesla MRI with abnormal enhancement of the left nasolabial fold and perineural tumor spread along the left infraorbital nerve to the left pterygopalatine fossa (Figure 2).

A lumbar puncture was performed; cerebrospinal fluid (CSF) was negative for malignant cells by flow cytometry, and the CSF findings are summarized in Table 1.

Isoelectric focusing (IEF) and immunoblotting were used to perform oligoclonal banding testing. One paired band and zero nucleated cells were found in both the CSF and serum, which indicates an inflammatory process outside the central nervous system. Zero oligoclonal bands were found in the CSF, which rules out an ongoing central nervous system inflammatory process.

A paraneoplastic panel including anti-acetylcholine receptor ganglionic neuronal antibodies, anti-amphiphysin antibodies, anti-glial nuclear antibody type 1, anti-neuronal nuclear antibody type 2, anti-neuronal nuclear antibody type 3, collapsing response-mediator protein-5 (CRMP-5) immunoglobulin G, neuronal voltage-gated potassium channel antibodies, calcium channel antibody P/Q-type, and Purkinje cell cytoplasmic antibodies were negative.A referral to the ear-nose-throat (ENT) specialist revealed no cervical adenopathy or neck masses. A computed tomography (CT) scan of the chest, abdomen, and pelvis did not reveal evidence of malignancy. The patient refused a facial nerve biopsy of a facial nerve twig of the parotid gland and other invasive procedures including a skin biopsy over the nasolabial fold. It was determined that the likely source of the malignant perineural spread along the skull base foramina (foramen rotundum and ovale) was dormant basal cell carcinoma cells. The patient received proton beam radiation therapy to the involved sites, including the maxillary region of the face, the involved sinuses, and the skull base.

Neoplastic involvement of the trigeminal nerve can cause TNp and can pathologically be attributed to nerve compression, perineural spread (PNS), and/or perineural invasion (PNI). Metastasis from breast or lung cancer to the Gasserian ganglion is rare, as is leptomeningeal metastasis, which is usually lymphomatous [8,10]. Carcinomatous leptomeningitis can affect other cranial nerves and can rarely present with an isolated TN and/or TNp [11].Most primary tumors of the trigeminal nerve are due to a schwannoma and rarely are due to meningioma, lipoma, or epidermoid tumor [12].

The peripheral and cranial nerves harbor three layers of connective tissue across their diameter: endoneurium, perineurium, and epineurium. The perineural space is located between the nerve axon and the perineural layer. This potential space can allow for tumor spread and growth. There are two types of perineural tumor growth: perineural invasion (PNI) and perineural spread (PNS). PNI is defined by malignant cells invading the perineural space and is a histological diagnosis. PNS is a radiological diagnosis of malignant spread along the nerve and is identified by enhancement detected by high-resolution MRI. During the initial stages of the disease, only PNI may be present. As disease progression occurs, PNI can become PNS, which is clinically more aggressive [13,14]. A patient with numbness to the territory innervated by the mental branch of the mandibular nerve should always raise a red flag. The mental branch is purely sensory in function and provides cutaneous innervation to the lower lip and chin. This characteristic numbness is aptly named the numb-chin syndrome. Malignant mental neuropathy can indicate the presence and/or recurrence of a malignant tumor [15]. Facial numbness that spreadsand radiates into the tongue, roof of the mouth, and inside the cheeks should raise a high index of suspicion for an inflammatory or malignant invasion of the trigeminal nerve.

Hence, perineural tumor spread of carcinoma may be seen along the maxillary and mandibular division of the trigeminal nerve. Nerve enhancement is one of the radiological findings in perineural tumor spread and can serve as a dependable sign. High-resolution MRI is the imaging modality of choice due to its ability to demonstrate soft tissue in high detail. MRI enhancement of the mandibular nerve in asymptomatic patients is very uncommon and was only seen in 3% of patient cases without symptoms of TNp. Therefore, when symptomatic maxillary or mandibular nerve enhancement is discovered on MRI, a high index of suspicion for an underlying disease process should be raised [16,17].

Perineural spread of head and neck cancers is a well-described phenomenon. At the cellular level, neural secretion of glial-derived neurotrophic factor (GDNF) may allow perineural spread. GDNF phosphorylates the rearranged during transfection (RET) tyrosine kinase receptor that triggers downstream signaling pathways that allow malignant cell migration [18]. Adenoid cystic carcinoma and squamous cell carcinoma are the most common malignancies that can spread perineurally [3]. Although not the most common, basal cell carcinoma has been described in the literature. However, very few cases exist where the only clinical manifestation of basal cell carcinoma recurrence is trigeminal neuropathy [19].

Additional etiologies of TNp include inflammatory, autoimmune, paraneoplastic, and infectious disorders. Inflammatory/autoimmune etiologies include sarcoidosis, Lymes disease, Sjogrens syndrome, and systemic lupus erythematosus [8]. Malignancies that can cause paraneoplastic syndrome include, but are not limited to, small cell lung cancer, breast cancer, ovarian cancer, and pancreatic cancer. TNp can be one of the first clinical manifestations of a paraneoplastic syndrome [20]. Infectious causes include leprosy, herpes simplex virus, varicella-zoster virus, actinomycosis, and aspergillus [8].

In conclusion, the diagnosis of trigeminal neuropathy should evoke a specific set of differential diagnoses. Since trigeminal neuropathy can be one of the first and only manifestations of a head and neck tumor, local malignant perineural invasion should be seriously considered. A high-resolution MRI of the skull base with and without gadolinium contrast enhancement should be ordered as our case demonstrates that a higher magnetic field strength can highlight pathology not seen with lower magnetic field strength MRI.

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A Case of Secondary Trigeminal Neuropathy Due to Local Malignant Invasion of the Maxillary and Mandibular Nerves at the Skull Base: A Case Report With...

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North America (United States, Canada and Mexico)

Europe (Germany, France, United Kingdom, Russia, Italy, and Rest of Europe)

Asia-Pacific (China, Japan, Korea, India, Southeast Asia, and Australia)

South America (Brazil, Argentina, Colombia, and Rest of South America)

Middle East & Africa (Saudi Arabia, UAE, Egypt, South Africa, and Rest of Middle East & Africa)

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Segment by Type Elamipretide GS-011 IXC-201 KH-176 OthersSegment by Application Hospital Clinic Others

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Alkeus Pharmaceuticals Inc., Biovista Inc., GenSight Biologics S.A., Ixchel Pharma LLC, Khondrion BV, Spark Therapeutics Inc., Stealth BioTherapeutics Inc.

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