Back Clinic Chiropractic. This is a form of alternative treatment that focuses on the diagnosis and treatment of various musculoskeletal injuries and conditions, especially those associated with the spine. Dr. Alex Jimenez discusses how spinal adjustments and manual manipulations regularly can greatly help both improve and eliminate many symptoms that could be causing discomfort to the individual. Chiropractors believe among the main reasons for pain and disease are the vertebrae’s misalignment in the spinal column (this is known as a chiropractic subluxation).
Through the usage of manual detection (or palpation), carefully applied pressure, massage, and manual manipulation of the vertebrae and joints (called adjustments), chiropractors can alleviate pressure and irritation on the nerves, restore joint mobility, and help return the body’s homeostasis. From subluxations, or spinal misalignments, to sciatica, a set of symptoms along the sciatic nerve caused by nerve impingement, chiropractic care can gradually restore the individual’s natural state of being. Dr. Jimenez compiles a group of concepts on chiropractic to best educate individuals on the variety of injuries and conditions affecting the human body.
Hormone testing can now be done by using top of the line integrative methods and techniques. There are multiple reasons and benefits for an individual to complete a hormone test. These tests have the ability to help a patient understand their cycle, testosterone/ estrogen levels, why they are tired upon waking or throughout their day, and more.
Precision Analyical, Inc. has discovered a way to use scientists who have extensive experience and coupled them with the most advanced analytical methods and instruments. This allows them to achieve the best results when it comes to the dutchtest.
What is D.U.T.C.H?
D.U.T.C.H stands for ” Dried Urine for Comprehensive Hormones” and is comprised of multiple tests designed by Precision Analytical Inc. Dried urine samples allow scientists to see an entire day of hormones and measure multiple different aspects. There are different D.U.T.C.H tests that can be completed depending on the patient’s needs.�
Dutch Complete– This is a comprehensive assessment of sex and adrenal hormones and their metabolites. This test measures progesterone, androgen, estrogen metabolites, cortisol, cortisone, cortisol metabolites, creatine, DHEA-S.�
Dutch Sex and Hormone Metabolites– This test is focused on testing progesterone, androgen, estrogen metabolites
Dutch Adrenal– This is important to measure because it controls the stress hormone and the levels in the body to help with energy upon waking. This test specifically measures cortisol, cortisol metabolites, creatinine, DHEA-S
Dutch OATS “Organic Acid Tests”-� This test will give insights to symptoms such as mood and fatigue. This test measures 9-OHdG, melatonin.
Dutch Plus– This test uses 5 saliva samples to provide the up and down pattern of cortisol and cortisone throughout the day. This test adds salivary cortisol measurements of the cortisol awakening response (CAR) to the dutch complete to bring another important piece of the HPA axis into focus
Dutch Test Cycle Mapping– This test maps the progesterone and estrogen pattern throughout the menstrual cycle. It provides the full picture of a woman’s cycle to answer important questions for patients with month-long symptoms, infertility, and PCOS. This test is targeted to measure 9 estrogens and progesterone that are taken throughout the cycle to characterize the follicular, ovulatory, and luteal phases.�
How Does It Work?
One of the reasons that many practicing offices are starting to use the D.U.T.C.H tests is because they have an extremely simple sample collection. Patients will collect just 4-5 dried urine samples over a period of 24 hours. This makes transportation and collection of the sample hassle-free. The dried urine samples provide excellent results due to the fact that the collections offer a span of the entires day hormones. The time of testing looks as follows:
The patient obtains the first sample at approximately 5pm ( dinnertime)
The� second sample is to be taken around 10 pm ( bedtime)
This next sample is dependent upon each individual, but if the patient wakes to urinate during the night, a sample is to be collected at this time.
The third sample should be collected within 10 minutes of rising. It is very important that the patient does not lay in bed after waking and they collect this sample within those allotted 10 minute time frame.
Once the patient has collected their third sample upon rising, they should set an alarm for 2 hours, as this is when the fourth and final sample is to be collected.
As one can see above, these urine samples will be dry when sent off to the lab. Studies show that dried urine samples are stable for weeks and will give an accurate representation of the hormone levels that are being assessed. From here, the results are gone over with a team of clinicians from Precision Analytical with the doctor who ordered the test. This ensures that the best treatment protocol is created for the patient.��
What Is The Purpose?�
With the turn around time being just 7-10 business days, individuals can gain control fairly quickly. As mentioned, Precision Analytical uses the most advanced instruments to achieve the best results for patients. The main purpose is to create an understanding of what is going on inside the patient’s body and allows the treatment to be more specific and targeted to the individual’s needs. As Chiropractic Health Month approaches, there is no better time than now to get started!�
�I highly recommend the D.U.T.C.H test. Knowing and understanding your hormones and the times that they are rising and falling throughout the day opens so many doors. It allows an individual to have an understanding of why they are so tired or why they can not fall asleep and take distinctive steps towards correcting that issue, rather than shooting in the dark. In addition, it allows patients to have knowledge of what is occurring when it comes to their sex hormone metabolites. This test gives the ordering doctor a complete look at the patient’s hormones and ensures they can be confident in creating a treatment protocol. – Kenna Vaughn, Senior Health Coach
The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
Sciatica doesn�t have to prevent you from being able to travel.
Sometimes a journey can create a series of challenges for people with sciatic nerve pain in the low back and leg.
A common issue among individuals is to prevent sciatica from flaring up when on the road or in the air.
A solution for this is to find ways to keep moving. However, easier said than done, but it can be done!
Flying and driving often mean long periods of sitting and sitting in a position typically not friendly with sciatic pain.
“When we drive or fly for an extended trip, it means long sitting times, and sitting in a position that can cause sciatica to flare up at any time,” says Dr. Alexander Jimenez, D.C. in El Paso, Texas, and member of the American Chiropractic Association (ACA).
Dr. Jimenez shares some basic tips for keeping mobility up, all the while pain-free, when flying and driving with sciatica.
He also offers additional advice to keep radiating pain from starting, upon arrival.
Flying with Sciatica
Sciatica pain radiates through the lower body meaning:
The low back
Hips
Buttocks
Legs
So when a flight anchors you to a seat, this can aggravate the area and cause pain.
The first thing to consider is the seat choice.
An aisle seat allows you the easiest access out of the seat, allowing you to move more during the flight.
Also when flying with sciatica, tell the flight crew about your condition.
When the seatbelt off light comes on, get up, stretch your legs and move around anywhere you can find room.
With a good portion of the population suffering from sciatica, most crews have seen people with this condition, and will usually let you do some stretching if they’re not busy.
A good sciatica stretch is to put your hands on something stable and do some deep knee bends.
This will use the upper body weight to stretch the lumbar spine comfortably.
Do a few and make sure you feel and return to your seat stretched and refreshed.
When taking a long flight, do this every hour to feel better when landing.
Sciatica Road Trip
Road trips, on the other hand, are easier to stop and move around. However, it can also create over-concentration on the drive and forgetting how much you are hurting until the pain is unbearable.
Dr. Jimenez advises frequentstops, if possible every hour is best to prevent pain.
On the stops walk two or three laps around the car/Suv/truck.
Rear bumper stretching prop
Place one foot on the bumper, and the other a few feet behind, lean into the bumper and square the hips with the lead foot.
This is like a hurdle stretch.
Stretch both legs on each break.
Regular stretching helps relieve the pressure on the low back so you can drive comfortably.
Arrival
Packing light is a healthy tip because hauling heavy luggage will aggravate sciatic nerve pain.
There are a few things that Dr. Jimenez recommends packing or getting upon arrival.
Gel ice pack you can keep in the refrigerator or freezer in a hotel.
Apply the cold pack to the low back for 20-minute increments will go a long way toward relieving pain.
Topical agent/cream/gel that has menthol or camphor, that you can apply to any area of tenderness or pain before the ice gel pack.
This increases the ice pack’s power by helping relax muscles and decreasing pain.
Supportive shoes or custom foot orthotics
People with sciatica should choose footwear or orthotics that support all three arches of the foot.
Leg length is usually not equal on each side, and proper arch supports can be custom made for you by your chiropractor to compensate for the difference.
Even a 5mm difference can cause chronic back pain.
And if possible, ask your chiropractor or primary physician if they can recommend a chiropractor, physical/massage therapist,� or acupuncturist that you can see in case you need emergency treatment.
This can give you some peace of mind.
Keep Your Exercise/Stretching Routine When Traveling
When we travel especially on vacations it can be easy to let healthy lifestyle habits you practice at home slide.
All are sciatica�s natural enemies make sure to bring these healthy practices with you to your destination.
Use the same good sense when you travel just like at home getting:
Get plenty of rest
Drink plenty of water
Don’t overeat
You will need more rest when you travel and don’t forget when you travel to:
Walk
Stretch
Stay mobile
Difference Foot Orthotics Make to *REDUCE FOOT PAIN* & Correct Posture | El Paso, TX (2019)
Custom made foot orthotics can help control foot motion and posture. Healthcare professionals prescribe custom foot orthotics to help patients focus on their foot posture and mobility control. Research studies have ascertained that using custom foot orthotics for posture and mobility control can help fix excessive foot pronation and supination to prevent a variety of foot health problems. The subsequent video describes how custom foot orthotics will help control foot posture and mobility to improve health and wellness.
NCBI Resources
Sciatica is generally caused by the compression of lumbar or sacral nerves or by compression of the sciatic nerve. When sciatica is caused by compression of a dorsal nerve root, it’s known as lumbar radiculopathy. This can occur because of a spinal disk bulge or spinal disk herniation (a herniated intervertebral disc), or by roughening, enlarging, or misalignment (spondylolisthesis) of the fascia, or as a consequence of degenerated discs which can reduce the diameter of the lateral foramen by which nerve roots exit the spine.
L-glutamate is one of the main excitatory neurotransmitters in the human brain and it plays an essential role in practically all activities of the nervous system. In the following article, we will discuss the general principles of L-glutamate signaling in the brain. Then, we will demonstrate this scheme by describing the different pools of extracellular glutamate, including the synaptic, the perisynaptic, and the extrasynaptic, resulting from vesicular and non-vesicular sources or abnormally located glutamate receptors outside of synapses as well as discuss their possible physiological functions in the human brain. �
Glutamate Signaling in the Brain
According to research studies, the human brain has about a 6 to 7 ?mol/g wet weight of L-glutamate. L-glutamate, together with glutamine, is one of the most abundant free amino acids in the central nervous system (CNS). More than five decades ago, several research studies demonstrated that L-glutamate has an excitatory response on nerve cells. Since then, its role as an excitatory neurotransmitter as well as its cerebral metabolism has been evaluated in numerous research studies. �
L-glutamate is commonly found throughout synaptic vesicles in the presynaptic terminal through the process of vesicular glutamate transporters. Additionally, several of the L-glutamate in the vesicles may develop by a vesicle-associated aspartate amino-transferase from 2-oxoglutarate utilizing L-aspartate as the amino group donor. During the depolarization of the presynaptic membrane, L-glutamate is released into the synaptic cleft and connects to ionotropic glutamate receptors, known as iGluRs, at the postsynaptic membrane, as shown in Figure 1. According to research studies, iGluRs are characterized as ligand-gated ion channels which include receptors of the ?-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), kainate, and N-methyl-D-aspartic acid (NMDA) types. While AMPA and kainate receptors primarily regulate and maintain sodium influx, NMDA receptors actually have a high calcium conductivity. Moreover, the activation of NMDA receptors plays a fundamental role in synaptic plasticity and learning. In contrast to the other iGluRs, the activity of NMDA receptors is ultimately restricted by an Mg+2 block at the regular membrane potential, however, the ion channel is immediately unblocked by membrane depolarization which eliminates Mg+2 from the pore. Furthermore, NMDA receptors are tetramers that have two NR1 subunits and two NR2 or NR3 subunits, according to several research studies. �
Additionally to iGluRs, there are also eight isoforms of metabotropic glutamate receptors (mGluRs) which belong to the family of G-protein-coupled receptors, where they don’t develop ion channels but instead signal through a variety of second messenger systems. L-glutamate-associated depolarization causes a postsynaptic excitatory potential which eases the development of an action potential at the axon hillock. The glutamatergic synapse is activated by astrocytic processes that demonstrate high levels of excitatory amino acid transporters (EAATs). There are five different EAATs, EAAT1 to 5, of which EAAT1 and 2 are the primary astrocytic EAATs, whereas EAAT3 shows a predominantly neuronal expression. Approximately 90 percent of the L-glutamate transport is regulated and maintained by EAAT2 such as GLT-1 in rodent models. These transporters then co-transport 2 or 3 molecules of Na+ and a proton with each molecule of L-glutamate or L-aspartate together with the counter-transport of a K+ ion. Therefore, by utilizing the electrochemical gradient of these ions throughout the plasma membrane as an energy source, the transporters are able to safely and effectively accumulate L-glutamate and L-aspartate in cells against their sudden intra- to extracellular concentration gradients. This allows the brain to control a very low extracellular L-glutamate concentration in the low micromolar range. It is generally believed that L-glutamate taken up by astrocytes is turned to glutamine by the enzyme glutamine synthetase, the glutamine is then released, taken up by neurons and turned to L-glutamate, where it is ultimately utilized once again for neurotransmission. �
Extrasynaptic Glutamate in the Brain
Aside from the essential role of L-glutamate as the primary excitatory neurotransmitter released from glutamatergic presynapses, as previously mentioned above, it has become evident that L-glutamate receptors outside the synaptic cleft also play an essential role in brain physiology. In the cerebellum, it was demonstrated by evaluating AMPA receptor-mediated currents in Bergmann glia that synaptically released L-glutamate concentrations can reach extrasynaptic concentrations of up to 190 ?M while concentrations in the synaptic cleft can exceed 1 mM. Moreover, several mGluRs have been shown to demonstrate a different localization in proximity to the postsynaptic density which would allow them to immediately recognize L-glutamate escaping from the synaptic cleft, as shown in Figure 1. However, current research studies have demonstrated that iGluRs, especially of the NMDA type, are also found at extrasynaptic regions in the neuronal cell membrane. Utilizing light and electron microscopy, other research studies also demonstrated that extrasynaptic NMDA receptors gather at different regions of close contact in the dendritic shaft with axons, axon terminals, or astrocytic processes. The proportion of extrasynaptic NMDA receptors was estimated to be as high as 36 percent of the dendritic NMDA receptor pool in rat hippocampal slices. Although extrasynaptic NMDA receptors were associated with similar scaffolding proteins as synaptic NMDA receptors, an in vitro research study suggested that extrasynaptic and synaptic NMDA receptors may ultimately activate different downstream signaling pathways with a variety of results, including the suppression of CREB activity by extrasynaptic NMDA receptor activation as well as activation by synaptic NMDA receptors. Furthermore, NMDA receptors localized extrasynaptically on dendritic shafts connect extrasynaptic L-glutamate as well as regulate and maintain Ca2+ influx during the elimination of the Mg+2 block by dendrite depolarization throughout the backfiring of action potentials. Research studies demonstrated that L-glutamate release from astrocytes can activate slow inward currents through extrasynaptic NMDAR receptors in CA1 neurons which can also be ultimately synchronized. The mechanisms through which glial cells release L-glutamate as well as how the extrasynaptic L-glutamate concentrations are controlled are vital towards understanding how the activity of extrasynaptic NMDA receptors is controlled. �
Different mechanisms through which astrocytes can release L-glutamate have been suggested, including vesicular L-glutamate release and non-vesicular release through anion channels as well as connexin hemichannels and release through the cystine/glutamate antiporter system x?c. Several research studies strongly suggest that vesicular release from astrocytes plays a minor role because the Ca+2-associated release of L-glutamate was still present in astrocytes created from dominant-negative SNARE mice where vesicular release can be blocked by doxycycline withdrawal. System x?c is a cystine/glutamate antiporter which is characterized as heterodimeric amino acid transporters, made up of xCT as the specific subunit and 4F2hc as the promiscuous heavy chain. This transporter is demonstrated in the brain, especially in astroglial and microglial cells, as shown in Figure 1. The fact that extrasynaptic L-glutamate levels in different regions of the human brain are downregulated by approximately 60 percent to 70 percent in xCT knock out mice, research studies demonstrated that system x?c releases L-glutamate into the extrasynaptic space and suggests that this transporter is essential in the regulation of extrasynaptic L-glutamate levels. This is further supported by the observation that when measured by in vivo microdialysis, the increase in extrasynaptic L-glutamate developed by EAAT inhibitors is neutralized by blocking system x?c while blocking neuronal vesicular L-glutamate release is ineffective. Further research studies are still required. �
Taken together, glutamatergic neurotransmissions don’t simply happen through classical excitatory synapses but also through extrasynaptic L-glutamate receptors, as shown in Figure 1. Finally, the levels of extrasynaptic L-glutamate are determined, at least partially, by glial non-vesicular L-glutamate release, as also shown in Figure 1. However, the regulation of extrasynaptic L-glutamate levels, as well as its temporal-spatial dynamics and its effect on neuronal function, neurodegeneration, and behavior, are far from being fully understood by researchers, healthcare professionals, and patients. �
Glutamate, together with aspartate, is one of the main excitatory neurotransmitters in the human brain. Although it plays a fundamental role in the overall structure and function of the nervous system, excessive amounts of glutamate can ultimately cause excitotoxicity which may lead to a variety of health issues, such as Alzheimer’s disease and other types of neurological diseases. The following article describes the role of glutamate in the human brain. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
L-glutamate is one of the main excitatory neurotransmitters in the human brain and it plays an essential role in practically all activities of the nervous system. In the article above, we discussed the general principles of L-glutamate signaling in the brain. Then, we demonstrated this scheme by describing the different pools of extracellular glutamate, including the synaptic, the perisynaptic, and the extrasynaptic, resulting from vesicular and non-vesicular sources or abnormally located glutamate receptors outside of synapses as well as discussed their possible physiological functions in the human brain. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Lewerenz, Jan, and Pamela Maher. �Chronic Glutamate Toxicity in Neurodegenerative Diseases-What Is the Evidence?� Frontiers in Neuroscience, Frontiers Media S.A., 16 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4679930/.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
�
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download �
* All of the above XYMOGEN policies remain strictly in force.
Myofascial syndrome, what is it? You’re probably thinking I don’t have that, but more than likely, you have.
Myo means muscle and fascia refer to the tissue bands that cover and connect the muscles/organs.
Tightness
Twitching areas
Painful knots
In the neck/back, then myofascial pain syndrome could be the cause.
Myofascial syndrome is a very common condition. It affects about 44 million people in the United States.
Trigger Points The Areas Where Pain Can Develop
Myofascial pain is associated with trigger points. These are areas that can become tender and stiff inside muscle tissue that reduce the range of motion.
Myofascial pain syndrome can happen when you have several active trigger points.
Trigger points are often referred to as knots because they feel tight and balled up compared to the softer relaxed surrounding muscle/s.
If the muscle becomes tight, it can cut off its blood supply, that can trigger:
Muscle tenderness
Pain
Spasm
Tightness
Trigger points can form all over the body which includes:
Neck
Mid-back
Low back
Common characteristics of trigger points are that they cause pain that travels or spreads to the surrounding area. For example, shoulder pain can radiate across the upper back.
The muscles can also twitch when touched.
Pretty much everyone has trigger points, but not all triggers cause symptoms.
Dormant or latent��trigger points can reduce the range of motion but only cause pain when directly palpated or compressed,
Active trigger points are painful any time, even when at rest.
Lifestyle factors like:
Stress
Poor posture
Can make a dormant trigger point become active.
Trigger Point Causes in the Spine
Spinal injury or trauma can result in myofascial pain syndrome, but lifestyle factors usually have a hand in the condition.
Poor posture over a long period, for example, sleeping in an awkward position can cause physical muscular stress on the spinal muscles.
Mental and emotional stress can present itself through muscle tension that helps the development of trigger points.
The trapezius muscle, that extends from the back of the neck down the shoulders and upper back, is the most common site of spinal trigger points and myofascial pain because of the significant amount of pressure that the muscle has to bear and its susceptibility to whiplash.
The Difference Myofascial Syndrome and Fibromyalgia
Because myofascial syndrome is linked to triggering points, fibromyalgia and its tender points bring out a comparison of the two.
Myofascial pain syndrome and fibromyalgia are two distinct conditions, and the table below outlines the primary differences.
Because they are unique conditions, there is a possibility to develop both conditions.
Doctor(s) can help craft a treatment approach that addresses the pain of both trigger points and tender points.
Diagnosis can be difficult
Myofascial pain syndrome is common but can be difficult to diagnose.
The challengingreasons behind diagnosing include:
Scientists are not sure how these trigger points cause pain.
The condition is often confused for other spinal disorders and conditions.
An example is having low back pain caused by myofascial syndrome in the lumbar spine. But low back pain brought on by arthritis can cause similar pain. That’s when the cause needs to be carefully and properly assessed.
There is no standard test for myofascial pain syndrome diagnosis yet.
There�s no standard diagnosing protocol but manual palpation or use of the hands to feel for:
Tenderness
Twitching
Tightness around the area
Is the most common way doctors diagnose the condition.
Some doctors might only utilize manual palpation but ultrasound is emerging as a diagnostic tool for myofascial pain syndrome.
Ultrasound produces clean images of the soft tissues and shows the active trigger points.
However, more research is needed to secure its place as a diagnostic method and tool.
A personal or primary care doctor can diagnose myofascial syndrome, but they may refer you to a pain specialist or a spine specialist like:
Doctors and researchers are still learning about myofascial syndrome, therefore, treatment options differ from doctor to doctor.
But most doctors do support a multidisciplinary treatment approach that is, using a variety of therapies and employing lifestyle changes to manage trigger point pain and prevent it from coming back.
Below are common treatments for myofascial pain syndrome.
Release Therapy
Myofascial release is a broad treatment option that consists of manual or instrument-guided therapydesigned to release the muscles and fascia by use of applying pressure.
Practitioners and clinicians are trained in myofascial release therapy, including:
Massage therapists
Physical therapists
Chiropractors
Physiatrists
The goal is the same:
Put pressure on the trigger point and release it.
Myofascial release technique might sound like a massage, but it is a distinct method compared to massage.
Massage moves muscles up and down,� myofascial release utilizes direct pressure into the stiff fascia and muscle.
Repeated pressure on the tight areas is not soothing, and patients tell of soreness during and after the treatment.
Once the trigger point loosens up, blood flow and nerve function begin to return to the area.
Then the pain is gone, hallelujah!
Additional Care Options
Myofascial release therapy is just one option for trigger point pain.
Other common treatments to manage spine-related pain include:
Home
If you know the location of the trigger points you can treat them at home with simple tools.
Rolling the trigger point over a:
Foam roller
Golf ball
Tennis ball
Can help loosen any of the tight areas.
Over-the-counter medication
If doctor-approved, then taking an over-the-counter pain reliever like acetaminophen (Tylenol) or ibuprofen (Motrin, Advil) can help with spine pain and allow daily activities.
Physical therapy
Physical therapy like:
Massage
Chiropractic
Heat
Electrical stimulation
Ultrasound
There are also stretches/exercises to keep muscles warm and flexible to help any future trigger points from forming.
Massage therapy
Licensed massage therapists practice myofascial release therapy, but also include other forms of massage
Deep tissue massage
Swedish massage
Can also help relieve trigger point pain.
Massage can also help to relax, and this is very important in preventing myofascial pain syndrome.
Also, learn how to keep stress and anxiety in check, and avoid tension that can turn into trigger points.
Dry needling/acupuncture
While both therapies use needles, dry needling and acupuncture are different treatments that can reduce the pain.
There is not a lot of research on dry needling like acupuncture, but it can help increase blood flow to the trigger point area.
Acupuncture means inserting needles into specific points on the body.
These needles help stimulate the body’s energy and help in sending signals to the nervous system to release chemicals into the body to help with the pain, which means less pain.
Trigger point injections
If any of these treatments don’t seem to be working, then you might want to talk to your doctor about trigger point injections.
Many people who have trigger points or myofascial pain syndrome in their spine have knots and tightness throughout their back and neck.
To prevent myofascial pain syndrome one needs to practice a healthy lifestyle that promotes good spine health.
Stretching and exercising regularly can help keep stress under control and prevent tension from building up, which makes it harder for trigger points to activate and cause pain.
El Paso Chiropractic Back Pain Therapy
Andres “Andy” Martinez first came to see Dr. Alex Jimenez in Push Fitness after undergoing back pain and knee issues. Following a period of physical therapy and rehabilitation, Andy became engaged in Crossfit, where he learned everything he needed to know about health and wellness from the coaches at Push. Andres Martinez expresses how grateful he is to receive the amount of care he does against the staff and he clarifies how much his perspective of fitness has shifted from the first time he walked into Push Fitness. Andy has seen a family at Push who led him to a healthy, clean life and both the trainers and staff mean everything to Andres Martinez.
NCBI Resources
The knots you have probably felt in your muscles or had others identify are also known as trigger points. These tight spots are often sensitive to the touch and can be found in any muscle in your body. As they develop, they may produce symptoms like numbness, burning, weakness, pain, and tingling. Trigger points are caused by trauma to the body, such as an accident in a car or during athletics. They can also be caused by more mild, long-term trauma, such as working at a desk without proper ergonomics or making a repetitive motion over a long period of time. Chiropractors are not only good at finding trigger points, but they are also good at treating them.
For people who love drinking diet sodas, recent research studies have found that diet drinks can increase the risk of stroke and dementia. Although diet drinks have been previously advertised as a much more healthier, low-calorie alternative than regular carbonated drinks, a closer look at the results of these recent research studies ultimately suggests otherwise. �
One research study, consisting of 2,888 participants, ages 45 and older, in the Framingham Heart Study, asked for diet entries to be filled out up to three times within a seven-year period. According to the research study, participants who said they drank one diet soda a day were roughly twice as likely to have a stroke within the next decade than individuals who didn’t drink diet soda. Drinking regular, sugar-sweetened carbonated drinks did not seem to increase the risk of stroke. �
However, these types of research studies have only been able to prove an association between diet drinks, stroke, and dementia. “Also, only 97 people (about 3 percent) had strokes during the follow-up, which means that only two or even three of those strokes may be associated to drinking diet soda,” stated Dr. Kathryn Rexrode, an associate professor of medicine at Harvard-affiliated Brigham and Women’s Hospital which co-authored a research study on soda intake and stroke risk. �
Risk of Stroke Associated with Diet Drinks
The research study found a slightly increased risk of stroke in people who drank more than one soda per day, whether or not it contained any type of artificial sweetener. Although the research study didn’t particularly show a considerable increase in stroke risk, that doesn’t necessarily suggest that they’re a better option than diet sodas. Research studies have shown that drinking carbonated drinks may lead to weight gain, diabetes, high blood pressure, heart disease, and stroke, ” she stated. �
As a matter of fact, researchers believe that one possible explanation as to why regular, sugar-sweetened carbonated drinks weren’t associated with stroke in the recent research study is a phenomenon known as the survival bias. In this instance, it would mean that individuals who drink a lot of carbonated drinks may have died from health issues such as heart disease. �
Conversely, diet drinks may be associated with an increased risk of stroke due to a variety of health issues known as reverse causation. In an attempt to be healthier, individuals who are overweight or have diabetes may be more inclined to select diet drinks over regular drinks. Their increased risk of stroke may come from their health issues rather than their drink option. “We may ultimately only be measuring the residual effect of weight gain, obesity, and diabetes,” says Dr. Rexrode. �
Artificial Sweeteners and Stroke
� Although researchers need further evidence to determine why artificial sweeteners may increase stroke risk, there are other reasons as to why these should be avoided. Research studies show that artificial sweeteners can make individuals crave sugary, high-calorie meals, therefore, decreasing the artificial sweetener’s purpose of cutting your total calorie consumption. �
Moreover, many researchers believe that people who use these artificial sweeteners, which can be many times sweeter than sugar, can come to find naturally sweet foods, such as fruits, to be less appealing and less-sweet foods, such as vegetables, to be entirely unpalatable. Furthermore, individuals may be missing out on the many nutrients found in fresh, natural foods. �
“I encourage my patients to stop drinking soda and other sugar-sweetened carbonated drinks regularly to prevent empty calories,” she says. “However, if someone says that they can’t do without soda in the morning to wake up, I will encourage them to switch to diet soda.” Water is a much better choice, however. “There are plenty of ways to make it more attractive, both visually and taste-wise.” She adds. Try flavoring sparkling or flat water or add crushed mint, cucumber, or frozen fruit. �
Risk of Dementia Associated with Diet Drinks
In another research study, people who drank diet soda were associated with an increased risk of developing dementia. “The research study can’t prove a connection between drinking habits and health issues, however, it does strongly suggest an association,” Stated Dr. Matthew Pase, neurology fellow at Boston University School of Medicine and contributing author. �
The initial research study evaluated food questionnaires, MRI scans, and cognitive tests of approximately 4,000 people ages 30 and up. Researchers found that individuals who consumed over three diet sodas per week were more likely to have memory problems, a reduced brain volume, and a smaller hippocampus, an area of the brain used in memory and learning. In the research study, drinking a minimum of one diet soda per day was also associated with a reduced brain volume. �
During a second research study, the researchers tracked two different groups of adults for ten years. According to the research study, out of almost 3,000 adults over age 45, approximately 97 adults suffered a stroke during that time and from almost 1,500 adults over age 60, approximately 81 adults developed Alzheimer’s disease or another type of dementia. �
Past research studies have connected diet drinks to an increased risk of weight gain and stroke. Researchers believe that artificial sweeteners may ultimately affect the human body in many different ways, such as by transforming gut bacteria and tricking the brain into craving more calories. This is the first-time diet sodas have been associated with dementia. Because people with diabetes drink more diet soda, researchers believe that the health issue may partly explain the rise in dementia, although not completely. When people with diabetes were excluded from the research study, the association stayed. �
As stated by the United States Department of Agriculture, Americans consumed 11 million metric tons of sugar in 2016, much of it in the form of sugary, sweetened carbonated drinks. Because it would have been difficult to measure total sugar consumption from all type of different food sources, the research study focused on sugary, sweetened carbonated drinks. �
A growing number of research studies suggest that diet drinks may not be a safe alternative to sugary, sweetened drinks. Even small causal effects can have much bigger consequences on health, given the popularity of both diet and regular sodas. The research study concluded that both glucose and artificially sweetened soft drinks “may be hard on the brain.” �
Diet soda is basically a mixture of carbonated water, natural or artificial sweetener, colors, flavors, and other food additives. Although diet drinks generally have very few to no calories, these essentially have no significant nutritional value. Many research studies have demonstrated that drinking diet soda is associated with an increased risk of stroke and dementia. Researchers have also found that diet drinks can cause a variety of other health issues. It’s essential for to avoid drinking too much diet soda. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Recent research studies have found that diet drinks are associated with an increased risk of stroke and dementia. Although diet drinks are advertised as a much more healthier, low-calorie alternative than regular carbonated drinks, a closer look at the results of these recent research studies ultimately suggests otherwise. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Corliss, Julie. �Does Drinking Diet Soda Raise the Risk of a Stroke?� Harvard Health Blog, 31 July 2017, www.health.harvard.edu/blog/drinking-diet-soda-raise-risk-stroke-2017073112109.
MacMillan, Amanda. �A Daily Diet Soda Habit May Be Linked to Dementia.� Health.com, 21 Apr. 2017, www.health.com/alzheimers/diet-soda-linked-to-dementia-stroke.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download�
* All of the above XYMOGEN policies remain strictly in force.
Cervical radiculopathy happens when a pinched nerve in the neck (cervical spine) causes pain.
Radicular pain can extend beyond the neck and radiate down:
The shoulders
Arms
Fingers
This type of nerve compression also causes:
Weakness
Numbness
Tingling
Reflex problems
The neck consists of 8 pairs of nerves that control several motor (strength) and sensory (feel) functions.
The cervical nerve roots at the top send movement and feeling signals to the head and neck, and the nerves at the bottom enable motor and sensory function to the arms and hands.
If one or more of the spinal nerves in the neck gets pinched, it can disturb its ability to function correctly.
This results in radiating pain in the neck and other areas of the body.
This condition can affect anyone but usually affects middle-aged adults.
Men also tend to develop cervical radiculopathy more than women.
Causes
The natural aging process on the spine is what usually causes cervical radiculopathy.
The spine goes through the aging process just like the rest of the body and even more as it is the basis of our structure.
This process can lead to several degenerative spinal disorders, that include:
Cervical spondylosis (osteoarthritis)
Spinal stenosis
Herniated discs
When nerve passageways begin to narrow, intervertebral discs begin to protrude,� and bone spurs, caused by these disorders can put pressure on the nerves in the neck.
The condition can also be caused by a traumatic injury to the neck like whiplash or sports injury.
Rarely is it caused by an infection or spinal tumor.
Symptoms
The primary symptom is pain radiating from the neck down to the:
Shoulders
Arms
Hands
Fingers
The above is an example of sensory function, which is related to feeling.
In addition to sensory symptoms, radiculopathy can also cause motor dysfunction.
Motor dysfunction relates to muscles and movement.
Reflex changes in the neck and upper body and weakness are examples of motor dysfunction.
Diagnosis
A spine specialist/chiropractor has several tools to diagnose cervical radiculopathy.
First and foremost your medical history will be reviewed and then will be:
Asked to describe symptoms
A physical exam will be conducted�to recreate the pain in a controlled manner in the:
Neck
Shoulder
Arms
Example: Spurling�s maneuver, which gently rotates the head, while applying gentle pressure.
Once the information from the medical history and physical exam are done,��imaging tests such as an MRI�may be ordered so they can pinpoint the location of the nerve compression.
MRI scans show the soft tissues in the spine, including the nerves.
The doctor may request a pair of diagnostic tests called electromyogram (EMG) and nerve conduction exam if there are significant upper nerve arm and neck pain.
These tests help understand if there is nerve damage, the cause of the damage and if the symptoms are related to the nerve damage.
EMG and nerve conduction tests are usually performed together to help in the diagnosis.
Emergency Symptoms
Once the spine specialist confirms the diagnosis, they will develop a treatment plan to relieve the nerve compression or prevent it from getting worse.
Most cases are taken care of with non-surgical treatment, however, if the following occurs you should contact your doctor:
Neck pain does not improve with treatment in the time your doctor expects.
Pain worsens regardless of treatment
Or you develop new:
Numbness
Weakness in the
Neck
Arms
Upper body
Develop fever
If you experience symptoms in the lower body like:
Weakness in the leg
Difficulty walking
Lack of bowel/bladder function, then seek medical attention immediately.
These symptoms may indicate cervical myelopathy, a more severe condition.
Cervical myelopathy is the compression of the spinal cord.
When the spinal cord gets compressed, it can generate widespread spine issues and usually requires surgery.
Treatment Cervical Radiculopathy
Like most types of spine pain, a doctor will recommend trying one or more conservative treatments first.
Conservative treatments are nonsurgical means.
It�s important to understand that just because a treatment is considered conservative does not mean it is ineffective.
In fact, it�s quite the opposite. Most people with nerve compression in their neck respond well to conservative therapies.
Though research on the efficacy of conservative treatments for cervical radiculopathy has produced mixed results, findings show that these therapies help eliminate pain and other nerve-related symptoms (like numbness and muscle weakness) in 40-80% of people.
The following are the most common conservative treatments:
Over-the-counter medications, like acetaminophen (Tylenol) or nonsteroidal anti-inflammatory medications(ibuprofen, Motrin)
Prescription medications, like steroids (prednisone), neuropathic agents (gabapentin, pregabalin), and muscle relaxants (baclofen, cyclobenzaprine)
Cervical spinal traction, that can be performed during physical therapy
Avoiding strenuous activity, but don’t avoid all activity, as too much rest can exacerbate the injury and extend the recovery time
These conservative treatments can go on for 6 to 8 weeks. If there is no improvement or it gets worse, then a doctor may want to step you up to the next level.
This may include steroid injections.
Spinal Injections
Cervical epidural steroid injections are considered a second-line treatment for radiculopathy that is not responding to conservative therapy. These injections send a dose of anti-inflammatory medicine into a specific nerve root�s that can relieve pain.
The number of injections differs from patient to patient. A doctor will make recommendations based on the condition and response to the first injection.
If the first injection reduces the pain and symptoms, a second or third injection might not be necessary unless symptoms recur.
If more than one is needed, they are given 3 weeks between each injection.
Injections can help manage pain and inflammation, but cannot strengthen or improve the flexibility of the cervical muscles.
Because of this, a doctor may prescribe physical therapy, chiropractic or an exercise program to condition the neck muscles.
Surgery Considered
When surgery is needed it is considered a last resort option. This is not a guaranteed solution and there are risks and complications.
Different types of surgical approaches are available. These procedures can be performed minimally invasively in a hospital setting or an outpatient surgery center.
Discussing options with a doctor and whether you are a candidate for minimally invasive surgery or not, along with other types of surgery e.g. artificial disc, is a discussion that is different for everybody, as some patients have existing medical conditions that can increase risks and complications.
Anterior cervical discectomy and fusion (ACDF)
This approach is the most widely used surgical approach.
The surgeon makes an incision through the front of the neck and removes the damaged intervertebral disc, fills the empty space with spacers to restore the height and attaches spinal instrumentation (plate, screws) for stabilization.
A bone graft is then packed into and around the body spacers for bone ingrowth and healing.
Posterior cervical foraminotomy
Here, the surgeon accesses one or more levels of the cervical spine with an incision in the back of the neck.
Foraminotomy decompresses the nerve root by removing whatever is compressing the nerve like a bone or soft tissue.
The procedure opens/widens the neural foramen or the nerve passageway where the nerve exits the spinal canal.
Cervical artificial disc replacement (C-ADR)
Here an artificial disc device is implanted in the empty disc space.
C-ADR is like a shock absorber and enables healthy movement the way that an actual disc does.
Conclusion
A compressed nerve in your neck can lead to radiating pain. This pain can make it almost unbearable to do simple tasks, even moving the neck from side to side or just opening a jar. Conservative treatment like chiropractic and exercise can ease the pain of this condition and restore function. Fortunately, surgery is rarely necessary.
El Paso, TX Neck Pain Chiropractic Treatment
Alfonso J. Ramirez now retired, found follow-up treatment with Dr. Alex Jimenez for his neck pain. Mr. Ramirez experienced chronic pain and headaches, but after receiving chiropractic care, he found relief from his symptoms. Ever since that time, Alfonso Ramirez has continued to maintain the alignment of his backbone with Dr. Jimenez. Mr. Ramirez is grateful for the chiropractic care he’s received for his neck pain and for his knee and shoulder pain. Alfonso J. Ramirez recommends Dr. Alex Jimenez as the non-invasive pick for neck pain.
NCBI Resources
Approximately two-thirds of the population being affected by neck pain at any time throughout their lives. Pain that originates in the cervical spine, or upper spine, can be caused by numerous other spinal health issues. Joint disruption in the neck can generate a variety of other common symptoms, which include headaches, head pain, and migraines. Neck pain affects about 5 percent of the global population, according to statistics.
Excitotoxicity is a pathological mechanism seen in a variety of health issues where an excessive synaptic excitation causes neuronal death and is also believed to be caused by the extracellular accumulation of the excitatory neurotransmitter glutamate, which triggers and connects ionotropic N-methyl-D-aspartate glutamatergic receptors (NMDARs) in the brain. Generally, NMDARs regulate and maintain calcium in cells to help manage physiological mechanisms like synaptic plasticity and memory, however, excessive stimulation can ultimately increase intracellular calcium which triggers cell death signaling to activate apoptosis. This pathological mechanism has been suggested in a variety of health issues, such as traumatic brain injury (TBI) and Alzheimer’s disease (AD), where it is extensively examined to understand health issues and treatment approaches. In a stroke, excitotoxicity has been shown to be the main pathological mechanism where neuronal damage happens and it is considered to be a well-known goal for many recent attempts at developing stroke therapeutics. �
Stroke is an acute brain health issue which causes neuronal damage which has currently no safe and effective neuroprotective treatment approaches. Immediately following a stroke, the brain tissue loses blood perfusion and the center of the infarct deteriorates quickly. This then causes milder ischemia and many brain cells or neurons will result in delayed death which can take up to several hours or even days. Research studies show that the mechanism of cell death is mainly NMDA receptor-dependent excitotoxicity. In ischemic areas, extracellular glutamate levels increase while preventing glutamate release, synaptic activity, or NMDAR activation which was capable of limiting cell death in a variety of stroke models. Thus, preventing excitotoxicity is an important treatment approach for reducing brain damage and improving patient outcome measures following a stroke, and this has definitely encouraged extensive efforts towards developing NMDA receptor-based stroke treatment approaches over the last two decades. Unfortunately, these have largely met with rather disappointing results. Several research studies have failed to find the expected efficiency of NMDAR for decreasing brain injuries. The reasons behind the basic research study results and clinical trials are still unknown, however, several reasons have been suggested. These include, but are not limited to, the inability to utilize the correct doses necessary for neuroprotection due to their side-effects, the inability to use the drugs within their neuroprotective windows, poor experimental designs, and heterogeneity in the patient population. However, as we will briefly summarize in the following article, improvement in our understanding of the physiological and pathological mechanisms of NMDAR activation as well as the different pathways connected to different NMDAR subtypes, has allowed researchers to develop new treatment approaches which improve therapeutic windows and increase specificity for death signaling pathways, achieving neuroprotection without interrupting other essential signaling pathways downstream of the NMDAR receptor. �
Neuroprotectants Targeting NMDAR Subtypes
NMDAR subtypes have different purposes in excitotoxicity and physiology. The NMDAR is a receptor which generally has two GluN1, also known as NR1, subunits as well as two subunits from the GluN2 subfamily (GluN2A-2D, also known as NR2A-2D). In the cortex, the major subpopulations of NMDARs are GluN2A- or GluN2A and 2B-containing receptors. GluN2A-containing receptors are found in synapses whereas GluN2B-containing receptors are found on extrasynaptic membranes. GluN2A- and GluN2B-containing receptors are different from each other because they regulate and manage plasticity, favoring either long-term potentiation (GluN2A) or depression (GluN2B) through a variety of electrophysiological and pharmacological properties as well as signaling proteins. In addition, these receptors play a fundamental role in promoting cell survival (GluN2A) or death (GluN2B) after excitotoxic stimulation. Because GluN2A-containing receptors are mainly focused on synapses while GluN2B-containing receptors are focused to both synaptic and extrasynaptic membranes, when excitotoxic conditions cause glutamate to extend beyond synapses, GluN2B-mediated death signaling becomes stronger in comparison to survival signaling which ultimately results in death. Through a stroke, by way of instance, NMDARs are less likely to favor cell survival and can instead cause detrimental effects by preventing considerable normal physiological purposes. Selfotel, a non-specific NMDAR blocker, was neuroprotective against stroke in vitro and in vivo, however, it ultimately failed to be neuroprotective against stroke in clinical trials by causing a variety of intolerable side-effects. �
Treatment strategies to reduce undesirable side-effects, including glycine site antagonists and NMDAR subtype-specific improvements, was to target the allosteric glycine binding regions on the GluN1 subunits with licostinel and gavestinel instead of directly blocking the receptor. These drug candidates performed well in preclinical examinations, however, they also failed as a result of low efficiency despite minimal side-effect profiles. The negative side-effects were perhaps due to a missed window of time following a stroke that shows which receptor blockers are safe and effective in preventing death. �
Better treatment methods and techniques for reducing unwanted side-effects of NMDAR are to utilize the differences between their variations. By way of instance, the GluN2B-specific inhibitor traxoprodil is neuroprotective in stroke research studies and minimal side-effects, however, it has also failed in clinical trials. Similar to the glycine region antagonists, it possibly needs to be properly regulated and managed to function efficiently. GluN2A agonists should promote cell survival signaling which could allow recovery following a stroke as well as cell survival to prevent passing signaling. As a matter of fact, activation of GluN2A-containing receptors utilizing increased doses of glycine was neuroprotective in an animal model of stroke but further research studies must examine GluN2A activation as a treatment approach in human participants. �
While NMDAR antagonists and modulators are safe and effective at attenuating excitotoxicity in experimental versions, their shortcoming is the challenge in implementing treatment approaches early to coincide with the summit of excitotoxic glutamate release. Stroke patients frequently have no chance of receiving these treatment approaches in time. However, the health issue can be avoided if receptor blockers can be utilized in at-risk populations. One research study has shown that low doses of prophylactic memantine, an NMDAR non-competitive antagonist with few side-effects, can considerably decrease brain injury and functional deficits following a stroke. Whether any medications are tolerable, safe, and effective when taken this way remains to be demonstrated but innovative solutions may nevertheless address how to deliver those drugs. �
One factor apart from those of the failed clinical trials is the interplay of NMDARs in cell survival which may be completely misunderstood. In the last few decades, there has been accumulating evidence that synaptic NMDARs may also cause cell death and GluN2A, as well as GluN2B, do not necessarily have dichotomous functions in excitotoxicity. Further research studies may be required to demonstrate more nuanced receptor inhibitor strategies and to solve this controversy. �
Neuroprotectants Targeting Cell Death Signaling
A treatment approach for NMDAR inhibitors is to focus on the most downstream events for cell death which happen over a much longer time period following receptor activation. A variety of cell death pathways following activation have been determined and several groups have provided proof-of-principle evidence that these pathways can be regulated and managed with the utilization of peptides to ultimately protect brain cells or neurons without any side-effects. �
The oldest reported and most explored peptide strategy in stroke goals is nitrous oxide synthase (nNOS)-mediated cell death. NNOS connects to postsynaptic protein 95 (PSD95) which then connects to the C-terminal tail of the GluN2B subunit. NOS is a calcium-activated enzyme which activates the development of nitric oxide (NO) and its own status in the receptor complex which associates it in proximity to the focused stream of calcium entering activated GluN2B. In a stroke, the excessive calcium influx activates GluN2B-coupled nNOS. An interference peptide is utilized to disconnect the complex to prevent NO development. The peptide, Tat-NR2B9c, is made up of an HIV-1 Tat-derived cell penetration sequence which allows passage through the blood-brain barrier and cell membranes, connected to a copy of the region on the GluN2B for PSD95. The peptide and GluN2B disconnect PSD95, therefore, decoupling nNOS in the local considerable levels of calcium without interrupting the function of the receptor from different pathways. Utilization results in considerable protection against tissue and functional damage with no side-effects in vitro and in vivo after a single dose given before or after ischemia in vivo. The peptide has lately succeeded in Phase II clinical trial where it decreased iatrogenic infarcts during intracranial aneurysm treatment. This is the first time a research study has demonstrated efficiency in humans which also shows authenticity that targeting downstream cell death can be helpful against excitotoxic/ischemic neuronal injuries. �
While the utilization of peptides in a clinical setting is safe and effective, a similar efficiency has been achieved with small molecule drugs which act on the exact same goal and function like the peptides in a laboratory setting. To mimic Tat-NR2B9c, two small molecules, IC87201 and ZL006 have been individually demonstrated to compete at the identical GluN2B-specific connecting region without affecting the connection of PSD95 to other proteins. Additionally, ZL006 imitates the peptide’s neuroprotection without causing any considerable adverse side-effects. By identifying the goals and the specific regions, research studies can simulate small molecule drugs and accelerate their discovery towards excitotoxicity and stroke. �
Other GluN2B-specific pathways have been demonstrated in a similar manner and are showing promise in the stages of development. One such pathway which is triggered following GluN2B activation is the potentiation and recruiting of GluN2B in the cell membrane by death-associated protein kinase 1 (DAPK1). DAPK1 is a protein which connects to calmodulin to activate apoptosis but it is phosphorylated in an inactive form which is incapable of associating cell death and calmodulin. Following excitotoxicity, calcineurin activation dephosphorylates and triggers DAPK1, contributing to cell death. Furthermore, active DAPK1 can connect to and phosphorylate the C-terminal tail of receptors, excitotoxicity, and their function, aggravating calcium influx. A Tat-linked interference peptide which has the C-tail phosphorylation region which is GluN2B managed to block the interaction of active DAPK1 with GluN2B and promote excitotoxicity. Once the peptide was utilized in mice, dubbed Tat-NR2B-CT, it improved the outcome following ischemia. However, Tat-NR2B-CT was only efficient at preventing activity and runaway insertion instead of the downstream apoptotic of DAPK1 signaling. Researchers were also able to connect and guide DAPK1 towards lysosomes by including a sequence in the close of the hindrance peptide to create a degradation peptide. The result has been a serious and temporary fall in busy DAPK1 levels with a corresponding decrease in infarction when administering the peptide hours after ischemia, according to several research studies. �
The c-Jun N-terminal kinase 3 (JNK) acts upon many pathways and is a mediator for cell death in excitotoxicity. JNK interacting protein (JIP) connects and prevents JNK activity through a JNK binding domain (JBD) which spans over 20 residues. When these residues are connected to Tat as from the Tat-JBD20 interrupted peptide, they are capable of limiting JNK activity and preventing cell death in stroke models when administered before or after ischemia. The Tat-JBD20 peptide has also been shown utilizing D-amino acids instead of L-amino acids to withstand degradation by endogenous proteases. Doing so tremendously increases the peptide’s half-life and doesn’t negatively affect its binding affinity and selectivity, demonstrating that this alteration may be utilized for several interference peptides to boost efficiency and bioavailability. �
New targets are always being discovered. While currently, no new stroke treatment approaches are being utilized, a great deal of progress has been made by targeting the processes which occur during stroke towards creating treatment approaches. With the debut of the achievement of degradation and interruption peptides targeting GluN2B-specific passing signaling events, there’s hope that new treatments are on the horizon for health issues which have excitotoxicity. �
Excitotoxicity is the pathological mechanism by which brain cells or neurons are ultimately damaged or eliminated by excessive stimulation from neurotransmitters, including glutamate and other similar substances. This ultimately occurs when the NMDA receptor and the AMPA receptor are overactivated by excitatory neurotransmitter glutamate receptors. This can cause a variety of processes which can damage cell structures, including components of the cytoskeleton, membrane, and DNA. Regulating and managing excitotoxicity can help maintain overall well-being. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Excitotoxicity is a pathological mechanism where an excessive synaptic excitation causes neuronal death and is also believed to be caused by the extracellular accumulation of the excitatory neurotransmitter glutamate, which triggers and connects ionotropic N-methyl-D-aspartate glutamatergic receptors (NMDARs) in the brain. This pathological mechanism has been suggested in a variety of health issues, such as traumatic brain injury (TBI) and Alzheimer’s disease (AD), where it is extensively examined to understand health issues and treatment approaches. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Li, Victor, and Yu Tian Wang. �Molecular Mechanisms of NMDA Receptor-Mediated Excitotoxicity: Implications for Neuroprotective Therapeutics for Stroke.� Neural Regeneration Research, Medknow Publications & Media Pvt Ltd, Nov. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC5204222/.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
�
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download �
* All of the above XYMOGEN policies remain strictly in force.
IFM's Find A Practitioner tool is the largest referral network in Functional Medicine, created to help patients locate Functional Medicine practitioners anywhere in the world. IFM Certified Practitioners are listed first in the search results, given their extensive education in Functional Medicine
