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Cyclists Benefit With Chiropractic | El Paso, TX.�

Cyclists Benefit With Chiropractic | El Paso, TX.�

Cyclists: Now that summer is upon us and the chilly winds of winter are gone for at least a few months, more people are taking their fitness and recreational activities outside. Cycling is popular activity that fits both bills. It is a great way to unwind and enjoy the great outdoors, but it is also an excellent form of exercise.

Cyclists

Chiropractic provides excellent benefits for the cycler, whether you hit the trails on the weekend, incorporate cycling as part of your fitness regimen, or commute to work on your bike every day.

  • Relief from Pain
  • Faster Healing from Injuries
  • Better Muscle Tone and Balance
  • Improved Range of Motion
  • Enriched Cycling Biomechanics

In short, chiropractic can help make you a better cyclist and help you get the most out of your cycling. It will help keep your body aligned and balanced physically, but it also treats the whole body.

That means that your chiropractor will also make nutritional recommendations and even recommend various supplements if necessary. This will give your energy a boost and improve your performance, while helping you stay healthy and fit. This is how chiropractic helps you have more stamina and endurance.

cyclists el paso tx.Chiropractic For Cycling Injuries

As with any type of physical activity, there is always a chance that injuries will occur. Chiropractic helps keep your body balanced and improves your flexibility. This, in turn, decreases your chance for injury.

However, if you are injured, chiropractic can help you recover and heal much faster. You start with a healthy, balanced body through regular chiropractic care, and that helps you bounce back faster if you sustain an injury.

Chiropractic care can also be used to treat injuries. Cycling can cause pain and injury in the ligaments, muscles, knees, ankles, hips, hands, wrists, feet, neck, back, and shoulders.

Regular adjustments can help decrease the likelihood of pain in these areas, but sometimes the soreness can creep in anyway. When that happens, chiropractic treatments have been shown to be very effective in treating pain without pain medication and associated harmful side effects.

Spinal alignment is one of the most common chiropractic techniques, but it goes much farther than that. Adjustments to the legs and feet can help with ankle, knee, hip, and foot pain. Adjustments to the arms and shoulders can help relieve pain in those areas. Special attention to the joints help keep them flexible and functioning as they should.

Chiropractic Allows The Body�s Natural Ability To Heal

Chiropractic is completely natural and does not rely on invasive treatments or surgeries. It does not use medications of any kind. It uses nutrition and supplements that rely on the body�s natural ability to heal. It simply realigns the body so that the neural pathways are unobstructed. This allows blood flow to be more efficient and reach the organs much easier.

Chiropractic involves gentle spinal manipulations that realign the body and restore movement in the joints as well as muscle trigger points and soft tissue. It may include electrical muscular current therapies, massage, cold laser therapy, ultrasonic waves, and other therapies in addition to the spinal manipulations.

A chiropractic patient may be advised to rest, ice an area, elevate it, or be given specific exercises to work that area. Chiropractic is not a rote therapy as many traditional medical practices tend to be. It adjusts to each patient, taking into account their unique lifestyle, activity level, nutritional needs, and other elements that influence that particular patient�s healing process.

Chiropractic sees each patient as individual and treat them as such. This is what makes it such an effective treatment for cyclists. The benefits it offers them can not only keep them pain free and participating in their activity; it can also make them better at it.

Injury Medical Clinic: Back Pain Care & Treatments

Chiropractic Benefits Those That Suffer From Migraine Headaches

Chiropractic Benefits Those That Suffer From Migraine Headaches

Chiropractic Benefits: If you have ever had a migraine before then you know that it is much more than a simple headache. The symptoms of a migraine can be debilitating, lasting hours and even days. According to the Migraine Research Foundation, it is the eighth most disabling disease in the world. It is estimated that 38 million people in the United States alone suffer from migraine headaches. That�s around one in every ten people.

According to the Migraine Research Foundation, migraine headaches are extremely difficult to treat and even more difficult to control. This is mainly due to the fact that doctors still don�t know exactly what causes it. This leaves it undiagnosed in many patients and often terribly under treated in those with a diagnosis.

The best many doctors seem to be able to do is prescribe pain medication that has undesirable side effects in an effort to manage the symptoms. However, chiropractic has been shown in several studies to not only effectively manage the pain of migraines, it also helps stop and prevent them.

Anatomy Of A Migraine Headache

There are two types of migraines, those with an aura and those without an aura. An aura can appear up to an hour before the onset of a migraine. It is a warning sign that usually presents as a disturbance that is either visual or olfactory. The person may see flashes of light or smell particular odors before the headache begins. About one in six migraines are preceded by an aura.

Once the migraine itself begins, the pain is typically on one side of the head, although this is not always the case. Other symptoms may include nausea, vomiting, sensitivity to noise, sensitivity to light, and sensitivity to smell. Some patients experience an inability to concentrate, hot or cold flashes, stiffness in neck or shoulders, slurred speech, loss of coordination, and in rare cases, loss of consciousness.

The migraine can last several minutes, hours, or even days. Afterwards the patient may feel fatigued or washed out. They may be unable to concentrate and either lethargic or extremely energetic.

Studies Show: Chiropractic As A Migraine Treatment

There have been several clinical studies on chiropractic as a treatment for migraine headaches. The results of one study reported that 22 percent of patients who received chiropractic treatment for their migraines reported that their attacks were reduced by more than 90 percent. Additionally, 49 percent reported that the intensity of their migraines was significantly reduced.

Another study randomly assigned people with migraine headaches several different treatments. One group was given Elavil, a daily medication, another group was given chiropractic treatment and a third group received a combination of the two treatments. The results showed that chiropractic was as effective in reducing migraines as the medication and it had fewer side effects. Other studies have also found that chiropractic is as effective as medication for the treatment and prevention of migraine or tension headaches.

Chiropractic Benefits For Migraines Headaches

Spinal adjustments are very effective as a treatment for migraines. The whole body approach of chiropractic also utilizes dietary recommendations, including foods to avoid, as well as lifestyle changes.

The patient may be counseled on managing stress, advised to engage in exercise, and given supplements. The treatments may be used to reduce the pain and severity of a migraine once it begins or it can be used to prevent migraines and reduce their frequency.

Chiropractic benefits everyone and is a safer treatment with fewer side effects than�prescription medications. Chiropractic is quickly becoming the treatment of choice for many migraine sufferers. As the studies show, it works! So if you or a loved one suffer from migraines, give us a call. Our Doctor of Chiropractic is here to help!

Injury Chiropractic Clinic: Migraine Treatment & Recovery

What is Ataxia? | El Paso, TX Chiropractor

What is Ataxia? | El Paso, TX Chiropractor

Ataxia is a medical term used to describe a lack of muscle control or coordination of voluntary movements, including everyday physical activities like walking or picking up objects. Often referred to as a symptoms of an underlying health issue, ataxia can affect various movements, causing difficulties with speech patterns and language, eye movement and even swallowing.

 

Persistent ataxia generally results from damage to the part of the brain which controls muscle coordination, known as the cerebellum. Many causes and conditions can lead to ataxia, such as alcohol abuse, certain drugs and/or medications, stroke, tumors, cerebral palsy, brain degeneration and multiple sclerosis. Inherited faulty genes have also been associated to lead to ataxia.

 

Diagnosis and treatment for ataxia depends largely on the cause and/or condition. Adaptive devices, including walkers or canes, can help patients with ataxia maintain their independence. Chiropractic care, physical therapy, occupational therapy, speech therapy and regular aerobic stretches and exercises can also help improve the symptoms associated with this health issue.

 

Symptoms of Ataxia

 

Ataxia is a health issue which can develop gradually over time or it can come on unexpectedly. As a symptom of a number of neurological disorders, ataxia may ultimately lead to:

 

  • Poor coordination
  • Unsteady walk along with a tendency to stumble
  • Difficulty with fine motor tasks, such as eating, writing or buttoning a shirt
  • Changes in speech
  • Involuntary back-and-forth eye movements, known as nystagmus
  • Difficulty swallowing

 

When to Visit a Doctor

 

In the instance that a patient is not aware of whether they may have an underlying health issue that causes ataxia, such as multiple sclerosis, it’s essential to visit a doctor immediately if the patient:

 

  • Loses equilibrium
  • Loses muscle coordination at a hand, leg or arm
  • Has difficulty walking
  • Slurs their speech
  • Has trouble swallowing

 

Causes of Ataxia

 

Damage, degeneration or loss of neural cells in the section of the brain which controls muscle coordination, or the cerebellum, often results in ataxia. The cerebellum is made up of two pingpong-ball-sized parts of folded tissue located at the base of the brain close to the brainstem. The right side of the cerebellum controls coordination over the right side of the body; the left side of the cerebellum controls coordination on the left side of the body. Diseases that damage the spinal cord and peripheral nerves which connect the cerebellum to the muscles can also lead to ataxia. Ataxia causes include:

 

  • Head trauma. Damage to the brain or spinal cord due to a blow to the head, such as in the case of an automobile accident, can cause acute cerebellar ataxia, which comes on unexpectedly.
  • Stroke. After the blood supply to part of the brain is interrupted or severely reduced, depriving brain tissue of nutrients and oxygen, brain cells die.
  • Cerebral palsy. This can be a general term for a group of disorders brought on by damage to a child’s brain during early development, before, during or shortly after birth, which affects the child’s ability to coordinate body movements.
  • Autoimmune diseases. Multiple sclerosis, sarcoidosis, celiac disease and other autoimmune conditions can cause ataxia.
  • Infections. Ataxia may be an uncommon complication of chickenpox and other viral ailments. It may manifest in the healing phases of the infection and can last for days or weeks. Generally, the ataxia resolves over time.
  • Paraneoplastic syndromes. These are rare, degenerative health issues triggered by the body’s own immune system’s reaction to a cancerous tumor, referred to as neoplasm, most frequently from lung, ovarian, breast or lymphatic cancer. Ataxia can appear months or years before the cancer is even diagnosed.
  • Tumors. A growth on the brain, cancerous, or malignant, or noncancerous, or benign, can also harm the cerebellum, leading to ataxia.
  • Toxic reaction. Ataxia is a possible side effect of certain drugs and/or medications, particularly barbiturates, like phenobarbital; sedatives, like benzodiazepines; as well as some kinds of chemotherapy. These are important to diagnose because the effects are usually reversible. Also, some drugs and/or medications can cause problems with age, which means a person may need to reduce their dose or discontinue its use. Alcohol and drug intoxication; heavy metal poisoning, such as from mercury or lead; and solvent poisoning, like from paint thinner, can also cause ataxia.
  • Vitamin E, vitamin B-12 or thiamine deficiency. Not getting enough of these nutrients, due to the inability to absorb them enough, alcohol misuse or other reasons, may also ultimately lead to ataxia.

 

For a number of adults that develop sporadic ataxia, no particular cause is found. Sporadic ataxia can take lots of forms, including multiple system atrophy, a progressive and degenerative disease.

 

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Dr. Alex Jimenez’s Insights

The cerebellum is the region of the brain which is in charge of controlling movement in the body. Electrical signals are transmitted from the brain through the spinal cord and into the peripheral nerves to stimulate a muscle to contract and initiate movement. Sensory nerves also gather data from the environment regarding position and proprioception. When one or more of these pathway components experiences a problem, it can subsequently lead to ataxia. Ataxia is a medical term utilized to describe the lack of muscle coordination when a voluntary movement is attempted. It can make any motion which requires muscles to function a challenge, from walking to picking up an object, even swallowing. Diagnosis and treatment can help manage and improve the symptoms associated with ataxia.

 

Diagnosis of Ataxia

 

If an individual has developed symptoms of ataxia, a healthcare professional may perform a diagnosis in order to look for a treatable cause. Besides running a physical examination and a neurological examination, including assessing a patient’s memory and concentration, vision, hearing, balance, coordination, and reflexes, your doctor might request lab tests, including:

 

  • Imaging studies. A CT scan or MRI of a patient’s brain might help determine possible causes of ataxia. An MRI can sometimes reveal shrinkage of the cerebellum and other brain structures in people with ataxia. It might also demonstrate other findings that are treatable, such as a blood clot or benign tumor, which may be pressing on the cerebellum.
  • Lumbar puncture (spinal tap). A needle is inserted into the lower spine, or the lumbar spine, between two lumbar bones, or vertebrae, to remove a sample of cerebrospinal fluid. The fluid, which surrounds and protects the brain and spinal cord, is transported to a laboratory for testing.
  • Genetic testing. A healthcare professional might recommend genetic testing to determine whether a child has the gene mutation which causes hereditary ataxia. Gene tests are available for many but not all of the hereditary ataxias.

 

Furthermore, diagnosing ataxia may depend on which system is affected. For instance,�if the health issue lies in the vestibular system, the patient will experience dizziness, possibly having vertigo or nystagmus. They may also be unable to walk in a straight line and when walking, they will tend to veer to one side. If the health issue lies in the cerebellar system, cerebellar gaits present with a wide-base and generally involves staggering and titubation. Patient will also have difficulty doing the Rhomberg�s test with their eyes open or closed, because they cannot stand with their feet together, as described below.

 

Testing the Vestibular System

 

Testing the vestibular system to determine the diagnosis of ataxia can include the Fakuda Stepping Test and the Rhomberg Test. The�Fakuda Stepping Test is performed by having the patient march in place with their eyes closed and their arms raised to 90 degrees in front of them. If they rotate more than 30 degrees, the test is considered to be positive. It’s important to note that the patient will rotate toward the side of the vestibular dysfunction. The Rhomberg Test will confirm a diagnosis of ataxia if the patient sways a different direction every time their eyes are closed, as this may indicate vestibular dysfunction.

 

Testing the Cerebellar System

 

Testing the cerebellar system to determine the diagnosis of ataxia can include the piano-playing test and the hand-patting test as well as the finger-to-nose test. The piano-playing test and hand-patting test both assess for dysdiadochokinesia. Also in both tests, the patient will have more difficulty moving the limb on the side of cerebellar dysfunction. With the finger-to-nose test, the patient may be hyper/hypo metric in movement and intention tremor may be reveled.

 

Joint Position Sense

 

In patients with changes to their joint position sense, conscious proprioception may be diminished, especially in elderly patients and patients with neuropathy. Patients with joint position sense losses often rely on visual information to help compensate. When visual input is removed or diminished, these patient�s have exaggerated ataxia.

 

Motor Strength and Coordination

 

If the patient has reduced frontal lobe control, they may end up with an apraxia of gait, where they have difficult with the volitional control of movement. Extrapyramidal disorders, such as Parkinson disease, result in the inability to control motor coordination. Pelvic girdle muscle weakness due to a myopathy in this instance will produce an abnormal gait pattern.

 

Gait Examination

 

 

Gait Deviations

 

 

Treatment for Ataxia

 

There’s no specific treatment for ataxia. In some cases, treating the underlying health issue often resolves the ataxia, such as quitting the use of drugs and/or medications that cause it. In other cases, such as ataxia that results from chickenpox or other viral infection, it’s likely to resolve on its own. A healthcare professional might recommend treatment to manage symptoms, such as pain, fatigue or nausea, or they may recommend the use of adaptive devices or therapies to help with ataxia. Chiropractic care is a safe and effective, alternative treatment option which focuses on the treatment of a variety of injuries and/or conditions associated with the musculoskeletal and nervous system. A chiropractor commonly uses spinal adjustments and manual manipulations to correct any spinal misalignment, or subluxation, which may be causing a patient’s symptoms. In addition, a doctor of chiropractic, or chiropractor, may also recommend a series of appropriate lifestyle modifications, including nutritional advice and exercise plans, in order to restore a patient’s strength, mobility and flexibility. Chiropractic care together with the proper fitness routine can help speed up the patient’s recovery process.

 

Adaptive Devices

 

Ataxia brought on by conditions like multiple sclerosis or cerebral palsy might not be curable. In that circumstance, a healthcare professional might have the ability to recommend adaptive devices. These can include:

 

  • Hiking sticks or walkers for walking
  • Modified utensils for eating
  • Communication aids for speaking

 

Other therapies

 

A patient with ataxia might benefit from particular therapies, including: physical therapy to help improve coordination and enhance mobility; occupational treatment to help with daily living activities, such as eating on their own; and speech therapy to improve speech as well as aid with swallowing.

 

Coping and Support

 

The challenges a person face when living with ataxia or with a child with the condition might make the patient feel lonely or it may contribute to depression and anxiety. Talking to a counselor or therapist may help. Or perhaps the patient may find encouragement and understanding in a support group, possibly for ataxia or for their specific underlying condition, such as cancer or multiple sclerosis.

 

Although support groups aren’t for everyone, they may be good sources of advice. Group members often know about the newest treatments and tend to share their own experiences. If you’re interested, your healthcare professional may be able to recommend a group in your area. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

Curated by Dr. Alex Jimenez

 

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Additional Topics: Sciatica

Sciatica is medically referred to as a collection of symptoms, rather than a single injury and/or condition. Symptoms of sciatic nerve pain, or sciatica, can vary in frequency and intensity, however, it is most commonly described as a sudden, sharp (knife-like) or electrical pain that radiates from the low back down the buttocks, hips, thighs and legs into the foot. Other symptoms of sciatica may include, tingling or burning sensations, numbness and weakness along the length of the sciatic nerve. Sciatica most frequently affects individuals between the ages of 30 and 50 years. It may often develop as a result of the degeneration of the spine due to age, however, the compression and irritation of the sciatic nerve caused by a bulging or herniated disc, among other spinal health issues, may also cause sciatic nerve pain.

 

 

 

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EXTRA IMPORTANT TOPIC: Chiropractor Sciatica Symptoms

 

 

MORE TOPICS: EXTRA EXTRA: El Paso Back Clinic | Back Pain Care & Treatments

Chiropractic Care Neck Pain Treatment | El Paso, TX. | Video

Chiropractic Care Neck Pain Treatment | El Paso, TX. | Video

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. Since then, Alfonso Ramirez has continued to maintain the alignment of his spine with Dr. Jimenez. Mr. Ramirez is grateful for the chiropractic care he’s received for his neck pain and for his shoulder and knee pain. Alfonso J. Ramirez recommends Dr. Alex Jimenez as the non-surgical choice for neck pain.

Chiropractic Care Neck Pain Treatment

Neck pain (or cervical Gia) is a frequent problem, together with two-thirds of the population experience neck pain at any time in their lives. Neck pain, although felt in the neck, can be brought on by many other spinal issues. Neck pain may arise because of muscular tightness in both the neck and upper back, or pinching of the nerves emanating from the cervical vertebrae. Joint disruption in the neck also creates pain, as does joint disruption in the top back. Neck pain affects about 5 percent of the global population as of 2010.

chiropractic care el paso tx.

We are blessed to present to you�El Paso�s Premier Wellness & Injury Care Clinic.

Our services are specialized and focused on injuries and the complete recovery process.�Our areas of practice include:Wellness & Nutrition, Chronic Pain,�Personal Injury,�Auto Accident Care, Work Injuries, Back Injury, Low�Back Pain, Neck Pain, Migraine Headaches, Sport Injuries,�Severe Sciatica, Scoliosis, Complex Herniated Discs,�Fibromyalgia, Chronic Pain, Stress Management, and Complex Injuries.

As El Paso�s Chiropractic Rehabilitation Clinic & Integrated Medicine Center,�we passionately are focused treating patients after frustrating injuries and chronic pain syndromes. We focus on improving your ability through flexibility, mobility and agility programs tailored for all age groups and disabilities.

If you have enjoyed this video and/or we have helped you in any way please feel free to subscribe and share us.

Thank You & God Bless.

Dr. Alex Jimenez DC, C.C.S.T

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Injury Medical Clinic: Chronic Pain & Treatments

Kids Diagnosed With ADHD | How Chiropractic Benefits | El Paso, TX.

Kids Diagnosed With ADHD | How Chiropractic Benefits | El Paso, TX.

Kids: Attention-deficit hyperactivity disorder (ADHD) is characterized by impulsivity and hyperactivity over a period of more than six months. Symptoms are usually noted and the condition can be diagnosed in children younger than 7 years of age.

It impacts kids socially and academically. According to the CDC, around 10 percent of children in the United States, age 5 to 17 years, has been diagnosed with ADHD. It is usually treated with medications that can have very serious, even frightening side effects. Chiropractic care has been proven to be an effective treatment for ADHD in children.

The Truth About ADHD Medication

The increasing prevalence of ADHD has led to the development of several drugs that are intended to treat the symptom�s conditions. Ritalin has long been the standard for treating ADHD. This drug is a schedule II controlled substance and its effects are frighteningly similar to cocaine and amphetamines.

What�s more, it has been linked to certain cardiac related conditions in young children. Adderall, another ADHD drug is very popular on the street and students in high school and college illegally sell it and use it. Emergency room visits due to Ritalin intoxication has been steadily increasing and is at the same level as ER visits that involve cocaine. Both Ritalin and Adderall, as well as many other ADHD drugs, are highly addictive and commonly abused.

Chiropractic For Kids Diagnosed With ADHD

Chiropractic care does not necessarily �treat� ADHD, but it does have very positive effects on children who have been diagnosed with the condition. There have been several studies that support how chiropractic helps ADHD. It is a safe, natural treatment for the condition and helps treating the symptoms. It goes far beyond treating back pain and neck problems. The adjustments can help a great deal.

The chiropractor will find subluxations in the spine and address them. Regular adjustments can help with more efficient and effective nerve flow. If the child has a spinal misalignment that could be the cause of the behavioral issues. Another popular theory is that an imbalance in the child�s muscle tone creates the brain activity to be out of balance. Adjusting the child�s spine restores balance to the brain and body.

Chiropractic also offers a whole body approach to wellness and that can help ADHD symptoms as well. The child may be exposed to a variety of sound and light frequencies as part of their therapy. The doctor may also recommend certain dietary changes and exercises. In many cases, eliminating certain foods from a child�s diet can cause many ADHD symptoms to subside or even disappear completely.

A chiropractor may have specific lifestyle changes:

  • Find out if the child as any allergies and address them
  • Eliminate additives, food dyes, preservatives, and sugar from the child�s diet
  • Avoid any stimulants like nicotine, alcohol, and certain medications while pregnant
  • Use unprocessed, natural foods and avoid all herbicides and pesticides
  • Avoid stress while pregnant; take time to relax

These changes can make a significant difference in the child�s behavior.

There is also an upper cervical technique that chiropractors use to realign the bones in the spine and skull. It is believed that when these bones are out of alignment it puts pressure on certain areas of the brain, resulting in the behavior issues. This treatment has a very good response rate in kids who have been diagnosed with ADHD.

Chiropractic care is a viable alternative to some of the more undesirable treatments for ADHD. It is easier on the child and healthier as well as safer. It will help them perform better in school and have better behavior at home. More parents are opting for chiropractic care instead of harmful drugs. It is a child�s best chance.

Injury Medical Clinic: Chiropractor Recommended

Repositioning Maneuvers to Treat BPPV in El Paso, TX

Repositioning Maneuvers to Treat BPPV in El Paso, TX

Benign paroxysmal positional vertigo, or BPPV, is a mechanical issue in the inner ear. It occurs when some of the calcium carbonate crystals (otoconia) that are normally embedded in gel at the utricle become dislodged and migrate to at least one of those 3 fluid-filled semicircular canals, where they are not supposed to be. When enough of these particles accumulate in one of the canals they interfere with the normal fluid motion that these canals utilize to sense head motion, causing the inner ear to send false signals to the mind.

 

Fluid in the semi-circular canals doesn’t normally react to gravity. However, the crystals do proceed with gravity, thereby shifting the fluid when it normally would be still. When the fluid moves, nerve endings in the canal are eager and send a message to the brain the mind is moving, even though it is not. This false information doesn’t match what another ear is sensing, together with what the eyes are seeing, or with what the joints and muscles are doing, and also this mismatched information is perceived by the brain as a turning sensation, or vertigo, which generally lasts less than one minute. Between vertigo spells some people today feel symptom-free, while some feel a mild sense of imbalance or disequilibrium.

 

A healthcare professional will execute a collection of tests and evaluations in order to properly diagnose the individual’s BPPV. Regular medical imaging (e.g. an MRI) is not helpful in diagnosing BPPV, because it doesn’t show the crystals which have moved to the semi-circular canals. But when someone with BPPV has their own head moved into a position that produces the dislodged crystals move within a tube, the error signals cause the eyes to move in a very specific pattern, called”nystagmus”.

 

How the Inner Ear Balance System Works

 

 

The nystagmus will possess distinct characteristics that let a trained practitioner to identify which ear the crystals that are displaced are in, and then canal(s) they have moved into. Tests such as the Dix-Hallpike or Roll Tests involve moving the head into specific orientations, allowing gravity to move the dislodged crystals and activate the vertigo while the professional watches for the tell-tale eye movements, or nystagmus.�To execute the Dix-Hallpike test, a healthcare professional will ask the patient to sit on the test table with their legs stretched out. They will then turn the head 45 degrees to one side, which contrasts the right posterior semicircular canal with the sagittal plane of the body, then they are going to allow the patient to lie back quickly, while the eyes are open, so that their head hangs slightly over the edge of the desk.

 

When the health care provider has finished the diagnosis, then they can perform the appropriate treatment maneuver. The maneuvers make use of gravity to guide the crystals back to the room where they are supposed to be via a very specific series of head movements, commonly referred to as Repositioning Maneuvers. Repositioning maneuvers are highly effective in treating BPPV, inexpensive, and easy to apply.

 

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Dr. Alex Jimenez’s Insights

While the use of surgical interventions as well as that of drugs and/or medications are occasionally recommended to relieve the symptoms associated with benign paroxysmal positional vertigo, or BPPV, they do not treat the underlying health issue. Repositioning maneuvers, like the ones demonstrated below, are considered to be safe yet effective treatment options for BPPV. There is good evidence to support the treatment of BPPV with the Epley maneuver. Although less amounts of research studies have been conducted on other repositioning maneuvers, outcome measures of a variety of patients with BPPV have benefitted from the other treatment options for benign paroxysmal positional vertigo.

 

Considering that the therapeutic efficacy among maneuvers for every canal is comparable, the option of treatment is generally predicated on clinician preference, complexity of their maneuvers themselves, therapy response to certain maneuvers, as well as musculoskeletal considerations, such as arthritic changes and range of motion of the cervical spine. Below, many repositioning maneuvers are demonstrated, for instance, deep mind hanging maneuver, the Lempert (BBQ) maneuver and the Epley maneuver.

 

Deep Head Hanging Maneuver for BPPV

 

 

The deep head hanging maneuver is a repositioning maneuver which is used for one of the least common places where BPPV occurs, the superior semi-circular canal, amounting to only about 2 percent of most benign paroxysmal positional vertigo instances. However, the advantage of deep head hanging maneuvers is that they may be effectively performed without knowledge of the side involved. It consists of three steps with four position changes at intervals of approximately 30 seconds.

 

The deep head hanging maneuver is performed with the patient at the long-sitting position, while the head is brought to a minimum of 30� below the horizontal with the head straight up. When the nystagmus induced by this measure is finished, the head is brought up rapidly to touch the chest while the patient remains supine, and after 30 seconds, the individual has been brought back to a seated position with head flexion maintained. Finally, the patient will be brought back to a neutral head position.

 

Lempert (BBQ) Maneuver for BPPV

 

 

The Lempert maneuver, also referred to as the Barbeque maneuver or the Roll maneuver, is a repositioning maneuver commonly utilized to help treat canilithiasis of the horizontal and lateral canal. It might occur as a complication of posterior canal BPPV treatment repositioning maneuvers. The side with the most notable horizontal nystagmus is assumed to be the affected side.

 

To perform the Lempert maneuver, the patient should lie supine on the exam table, using the affected ear facing down. Afterward, the healthcare professional will quickly turn the head 90� towards the unaffected side, facing up, waiting 15-20 minutes between each head turn. The medical professional will subsequently turn the head 90� so the affected ear is currently facing up. The next step includes having the individual tuck their arms to their torso, in order to allow the doctor to roll the patient to a more moderate position with their head down. The individual must be turned on their side since the physician rolls their head 90� (returning them to their original position, with the affected ear facing down ). At length, the medical professional should place the patient so that they are face up and bring them into a sitting posture.

 

Treatment with the Lempert maneuver is efficient approximately 75% of the moment, however, the effectiveness can vary from individual to individual. It is important to keep in mind that longer periods of time between head turns may provoke nausea. This sort of repositioning maneuver shouldn’t be done on patients in which it isn’t safe to move their mind, including in the case of cervical spine injuries.

 

Epley Maneuver for BPPV

 

 

The most common repositioning maneuver for the treatment of benign paroxysmal positional vertigo, or BPPV, is known as the Epley maneuver. The Epley maneuver, occasionally referred to as the canalith repositioning maneuver, is a process which involves a series of head movements, normally performed by a healthcare professional who’s experienced and qualified in the treatment of vestibular disorders, so as to relieve the symptoms associated with BPPV, including dizziness.

 

The Epley maneuver is performed by placing the patient’s mind at an angle in where gravity can help alleviate the symptoms. Tilting the mind can move the crystals out of the semicircular canals of the inner ear. This means that they will quit displacing the fluid, relieving the dizziness and nausea they may have been causing. In this manner, the Epley maneuver alleviates the symptoms of BPPV. But, it may have to be repeated more than once, as occasionally, some head movements can once again displace the small crystals of the internal ear, once they had been repositions after the first treatment.

 

Research studies have shown that the Epley maneuver is a safe and effective treatment for the specific vertigo disorder, offering both long-term and immediate relief. The Epley maneuver, named after Dr. John Epley, has been named the canalith repositioning maneuver because it helps to reposition the small crystals at a person’s inner ear, which might be causing the sensation of dizziness.

 

Repositioning these tiny crystals called otoconia helps to ease BPPV symptoms.�There are two types of BPPV: one where the loose crystals can move freely in the fluid of the canal (canalithiasis), and, more rarely, one where the crystals are thought to be �hung up� on the bundle of nerves that sense the fluid movement (cupulolithiasis).�It is important to make this distinction, as each repositioning maneuver may affect each variant differently. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

Curated by Dr. Alex Jimenez

 

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Additional Topics: Sciatica

Sciatica is medically referred to as a collection of symptoms, rather than a single injury and/or condition. Symptoms of sciatic nerve pain, or sciatica, can vary in frequency and intensity, however, it is most commonly described as a sudden, sharp (knife-like) or electrical pain that radiates from the low back down the buttocks, hips, thighs and legs into the foot. Other symptoms of sciatica may include, tingling or burning sensations, numbness and weakness along the length of the sciatic nerve. Sciatica most frequently affects individuals between the ages of 30 and 50 years. It may often develop as a result of the degeneration of the spine due to age, however, the compression and irritation of the sciatic nerve caused by a bulging or herniated disc, among other spinal health issues, may also cause sciatic nerve pain.

 

 

 

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EXTRA IMPORTANT TOPIC: Chiropractor Sciatica Symptoms

 

 

MORE TOPICS: EXTRA EXTRA: El Paso Back Clinic | Back Pain Care & Treatments

Ankle Pain | How Chiropractic Helps Resolves It | El Paso, TX.

Ankle Pain | How Chiropractic Helps Resolves It | El Paso, TX.

Ankle pain and injury are not issues reserved solely for athletes. In the United States, more than 25,000 people deal with ankle sprains or pain every day. Studies show that somewhere around 40 percent of ankle sprains are not treated correctly or are misdiagnosed, which leads to disability or chronic ankle pain.

When the ankle does not function properly, it can affect the entire body. The muscles on either side of the leg or even under the foot can become sore or painful. This can lead to loss of mobility, an uneven gait, and hip and back pain.

Anatomy Of The Ankle

Three bones connect to the joint that is the ankle. The lower ends of the tibia (shinbone) and the fibula (lower leg small bone) meet to form a socket that the talus (ankle bone) sits in.

The bottom of the talus rests on the calcaneus (heel bone). There is about an inch-thick lining of somewhat soft cartilage in the joint, which provides shock absorption for carrying body weight, but it is tough and durable so that, provided there is no injury, it will last for a lifetime.

The bones are held together by ligaments and the muscles are attached to the bones by tendons. When there is an injury, it can impact the bone, muscles, tendons and ligaments.

Treatment For Ankle Injury & Pain

The typical treatment for pain, such as with a sprain, is R.I.C.E., which is rest, ice, compression and elevation. A somewhat newer treatment approach replaces the R with an M, meaning that instead of rest, movement is required instead.

However, it is important that the movement is done safely and carefully. Certain types of ankle injuries can be exacerbated by movement so it should be approached with care.

Other types of traditional treatment include varying methods of pain control from ibuprofen to opioids. Severe injuries, such as a torn ligament, may require surgery. When a patient experiences pain, an x-ray is often used to see if there is an injury and to determine the extent of that injury. Sometimes, though an x-ray is not able to see the injury. In such cases, an MRI may be used.

ankle el paso tx.Chiropractic For Ankle Pain

Chiropractic is very effective for treating foot and ankle pain. The chiropractor will begin by assessing the patient�s source of pain and determine what is causing it. They may use x-rays, MRI, CT scan, and other types of diagnostic tools to help them select the best course or treatment.

When an injury is new and the area is inflamed and tender, the course of treatment may include ultrasound, iontophoresis and whirlpool baths. This is in addition to rest, ice, compression and elevation. As it heals, the inflammation subsides and it becomes more stable, chiropractic adjustments to the foot may be introduced.

Chiropractic can help reduce pain without prescription medication and the associated side effects. This alone is often a great draw for many patients. However, there are other benefits that chiropractic can provide for ankle pain.

Regular chiropractic treatment can help strengthen the ankle and increase its stability while increasing mobility and flexibility. Often nerves and soft tissue can become damaged. Chiropractic treatments done on a consistent basis facilitates blood flow, which speeds healing and reduces the chance of injury. It also uses a whole body approach so that the patient can get recommendation on diet and lifestyle changes, such as losing weight or exercising.

Chiropractic care is a very effective therapy for treating ankle pain and injury. It is non-invasive and a natural approach to healing that allows the body to heal itself.

Injury Medical Chiropractic Clinic: Migraine Treatment & Recovery

Auto Accident Injuries Chiropractor | El Paso, TX. | Video

Auto Accident Injuries Chiropractor | El Paso, TX. | Video

Auto Accident Injuries: Alfonso J. Ramirez, retired, has been pursuing a life full of health and wellness. Before he began following this type of lifestyle, however, Mr. Ramirez was hit by a car and suffered many injuries. He was treated accordingly at the time but was then referred to Dr. Alex Jimenez for chiropractic care. Once he received his first spinal adjustment, Alfonso Ramirez experienced tremendous relief from his symptoms. Grateful for all the medical services he’s been provided with, Mr. Ramirez expresses how Dr. Jimenez has helped restore his quality of life. Alfonso J. Ramirez recommends Dr. Alex Jimenez as the non-surgical choice for a variety of injuries and conditions.

Auto Accident Injuries Chiropractor

Millions of people are injured in automobile accidents every year, and many of these incidents can unfortunately result in long-term injuries and disability. Even if you are not in immediate pain following a car crash, seeking prompt chiropractic care may help prevent years of chronic pain. Chiropractic care is among one of the most popular ways for treating auto accident injuries. Chiropractic adjustments correct misalignments in the spine and help restore normal function to the nervous system so that the body can heal naturally. A chiropractor can help cure auto accident injuries without drug use. Also, chiropractic care can help with recovery without surgery.

auto accident injuries el paso tx.We are blessed to present to you�El Paso�s Premier Wellness & Injury Care Clinic.

Our services are specialized and focused on injuries and the complete recovery process.�Our areas of practice include:Wellness & Nutrition, Chronic Pain,�Personal Injury,�Auto Accident Care, Work Injuries, Back Injury, Low�Back Pain, Neck Pain, Migraine Headaches, Sport Injuries,�Severe Sciatica, Scoliosis, Complex Herniated Discs,�Fibromyalgia, Chronic Pain, Stress Management, and Complex Injuries.

As El Paso�s Chiropractic Rehabilitation Clinic & Integrated Medicine Center,�we passionately are focused treating patients after frustrating injuries and chronic pain syndromes. We focus on improving your ability through flexibility, mobility and agility programs tailored for all age groups and disabilities.

If you have enjoyed this video and/or we have helped you in any way please feel free to subscribe and share us.

Thank You & God Bless.

Dr. Alex Jimenez DC, C.C.S.T

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Injury Medical Clinic: Accident Treatment & Recovery

Cutting Your Nerve Changes Your Brain | El Paso, TX.

Cutting Your Nerve Changes Your Brain | El Paso, TX.

Following upper limb peripheral nerve transection and surgical repair, some patients regain good sensorimotor function while others do not. Understanding peripheral and central mechanisms that contribute to recovery may facilitate the development of new therapeutic interventions. Plasticity following peripheral nerve transection has been demonstrated throughout the neuroaxis in animal models of nerve injury. However, the brain changes that occur following peripheral nerve transection and surgical repair in humans have not been examined. Furthermore, the extent to which peripheral nerve regeneration influences functional and structural brain changes has not been characterized. Therefore, we asked whether functional changes are accompanied by grey and/or white matter structural changes and whether these changes relate to sensory recovery? To address these key issues we (i) assessed peripheral nerve regeneration; (ii) measured functional magnetic resonance imaging brain activation (blood oxygen level dependent signal; BOLD) in response to a vibrotactile stimulus; (iii) examined grey and white matter structural brain plasticity; and (iv) correlated sensory recovery measures with grey matter changes in peripheral nerve transection and surgical repair patients. Compared to each patient�s healthy contralesional nerve, transected nerves have impaired nerve conduction 1.5 years after transection and repair, conducting with decreased amplitude and increased latency. Compared to healthy controls, peripheral nerve transection and surgical repair patients had altered blood oxygen level dependent signal activity in the contralesional primary and secondary somatosensory cortices, and in a set of brain areas known as the �task positive network�. In addition, grey matter reductions were identified in several brain areas, including the contralesional primary and secondary somatosensory cortices, in the same areas where blood oxygen level dependent signal reductions were identified. Furthermore, grey matter thinning in the post-central gyrus was negatively correlated with measures of sensory recovery (mechanical and vibration detection) demonstrating a clear link between function and structure. Finally, we identified reduced white matter fractional anisotropy in the right insula in a region that also demonstrated reduced grey matter. These results provide insight into brain plasticity and structure-function-behavioural relationships following nerve injury and have important therapeutic implications.

Keywords: cortical thickness; fMRI; diffusion tensor imaging; plasticity; peripheral nerve injury
Abbreviations: BA=Brodmann area; BOLD=blood oxygen level dependent; fMRI=functional magnetic resonance imaging;
PNIr=peripheral nerve transection and surgical repair; S1=primary somatosensory cortex; S2=secondary somatosensory cortex

Introduction

Following upper limb peripheral nerve transection and surgical repair (PNIr), ?25% of patients have not returned to work 1.5 years after surgery (Jaquet et al., 2001). In addition, ?57% of patients with nerve injuries are between 16�35 years of age (McAllister et al., 1996); thus, a long life of disability and economic difficulties may accompany upper limb nerve transection. Understanding the central and peripheral ramifications of peripheral nerve injury may facilitate the development of new therapeutic strategies and intervention programs.

It is not known how the brain responds to PNIr in humans. However, animal studies have established that plasticity within the somatosensory cortex begins immediately following peripheral nerve transection, and that 1 year after complete nerve transection and surgical repair, cortical maps contain patchy, non- continuous representations of the transected and adjacent nerves (Wall et al., 1986). The mechanisms that facilitate functional plasticity are thought to include the immediate unmasking of pre-existing projections from adjacent cortical and subcortical levels, and long term sprouting of axons at multiple levels of the neuroaxis, including the primary somatosensory cortex (S1) (Florence and Kaas, 1995; Hickmott and Steen, 2005).

Human brain imaging studies have corroborated the findings from animal models with the identification of altered functional MRI activation maps due to spinal cord injury, amputation, toe- to-thumb transfer, and in patients with carpel tunnel syndrome (Lotze et al., 2001; Manduch et al., 2002; Jurkiewicz et al., 2006; Napadow et al., 2006). Furthermore, structural MRI studies have recently visualized grey and white matter changes following traumatic injuries and in diverse pathological conditions, including limb amputation and chronic pain (Apkarian et al., 2004; Draganski et al., 2006; Davis et al., 2008; Geha et al., 2008; May, 2008). Grey matter changes are thought to be related to changes in cell size, atrophy and/or loss of neurons or glia, whereas white matter changes are impacted by axonal degenera- tion and loss of myelin (Beaulieu, 2002; May, 2008).

A powerful approach to delineate mechanisms of pathology and plasticity is to combine functional and structural grey and white matter imaging techniques. We previously reported that patients with complete upper limb PNIr retained profound somatosensory deficits that persist 41.5 years following surgery (Taylor et al., 2008a). Based on these findings, we reasoned these patients would exhibit functional and structural brain changes in key somatosensory brain areas. Therefore, in this study, we hypothesized that PNIr patients would have: (i) reduced blood oxygen level dependent (BOLD) responses to vibratory stimulation of the transected nerve territory, in the region of S1 that represents the injured upper limb and in the secondary somatosensory cortex (S2); (ii) a corresponding reduction in cortical thickness in these regions of the contralesional S1 and S2; (iii) a correlation between changes in cortical thickness and psychophysical measures of somatosensory function (vibration and touch detection thresh- olds); and (iv) reduced fractional anisotropy (a measure of white matter integrity) in white matter feeding into/out of these somatosensory cortical areas.

Methods

Subjects

We recruited 27 patients with complete transection of the median and/or ulnar nerve followed by surgical repair from plastic surgeons affiliated with the University of Toronto Hand Program between June 2006 and May 2008. From this larger cohort, 14 pain-free patients (three females, 11 males; 34 ? 10 years) with complete transection of the right median and/or ulnar nerve were included in the study [to avoid confounds related to the presence of pain and laterality patients with pain (n=6) and left sided lesions (n=7) were excluded from this analysis]. All patients underwent microsurgical nerve repair at least 1.5 years prior to study enrolment (recovery time varied from 1.5 to 8 years). In addition, we recruited 14 age- and sex-matched healthy controls (3 females, 11 males; 34 ? 10 years). All subjects gave informed written consent to procedures approved by the University Health Network Research Ethics Board. All subjects were right handed (determined using the Edinburgh handedness inventory: Oldfield, 1971) and had no history of neurological injury or chronic pain (either before or after nerve transection). See Table 1 for demographic details.

nerve el paso tx.

Study Design

All subjects participated in an imaging session that included: (i) functional magnetic resonance imaging (fMRI) in response to vibrotactile stimuli applied to the right index finger (within the median nerve territory); (ii) a high-resolution anatomical scan of the whole brain, acquired for image registration and for the analysis of cortical grey matter; and (iii) two diffusion tensor imaging scans for the assessment of white matter integrity. Prior to imaging, subjects were instructed in the basic design of the experiment and reminded to remain as still as possible throughout the duration of the scan.

Subjects were free to withdraw from the study at any time. In addition, a sensory and motor assessment was performed for all subjects (Taylor et al., 2008a). As touch and vibration detection thresholds were correlated with cortical thickness a description of these methods is included below (other psychophysical measures will be reported elsewhere).

Vibration Threshold

Vibration detection thresholds were determined using a hand held Bio-Thesiometer (Bio-Medical Instrument Company, USA). The device has a 12-mm probe that was placed on the distal phalanx of the right index finger (D2). Thresholds were determined using the method of limits: the amplitude (voltage) was gradually increased until the subject indicated that they perceived the stimulus. Vibration thresholds were acquired three times and an average value was calculated. During vibration threshold testing, subjects were instructed to close their eyes and rest the back of their hand on a supportive cushion.

Mechanical Detection Threshold

Mechanical detection thresholds were determined using a standardized set of von Frey filaments (OptiHair2 Marstock Nervtest, Germany) containing 12 logarithmically spaced calibrated filaments that delivered forces from 0.25�512 mN. The contact surface diameter of all 12 filaments was ~0.4mm. Trials were conducted with the subject�s eyes closed and hands resting on a soft cushion. Probes were applied in an ascending series and subjects were required to make a response every time they felt a probe touch the right D2 fingertip. This process was repeated three times. The force for the filament that was detected in at least two of three trials was reported as that subject�s mechanical detection threshold.

Nerve Conduction Testing

Patients participated in bilateral sensory and motor nerve conduction studies at the Toronto Western Hospital electromyography (EMG) clinic. For motor nerve conduction, the stimulating electrode was placed at the wrist and elbow (separately) and the recording electrode was placed over the abductor pollicis brevis, for median nerve assessment, or the abductor digiti minimi for ulnar nerve assessment. For sensory nerve testing the recording electrode was placed at the wrist and the stimulating electrode was placed at digits D2, D3 and D5. A senior, experienced neurologist from the Toronto Western Hospital EMG Clinic (Dr Peter Ashby) reviewed all clinical assessments to deter- mine which nerves demonstrated normal/abnormal responses. As amplitude and latency measures are known to vary substantially between subjects (due to factors such as the density of innervation, the depth of the nerve and the thickness of an individual subject�s skin) (Kimura, 2001) each patient�s untransected nerve served as their own control for comparison with values from the transected side. In those patients with detectable nerve conduction responses, paired t-tests were performed to assess the difference in latency or amplitude measures between each patient�s transected and contralesional untransected nerves.

Imaging Parameters

Brain imaging data were acquired using a 3T GE MRI system fitted with an eight-channel phased array head coil. Subjects were placed supine on the MRI table and each subjects� head was padded to reduce movement. Whole-brain fMRI data was acquired using echo planar imaging (28 axial slices, field of view (FOV) = 20 x 20 cm, 64 x 64 matrix, 3.125 x 3.125 x 4mm voxels, echo time (TE) = 30 ms, repetition time (TR) = 2000 ms). The scan time was 5 min and 8 s (154 frames). During scanning, a non-painful, 12 Hz vibrotactile stimulus was applied to the distal phalanx of the right D2 using balloon diaphragms driven by compressed air (Device man- ufactured by Dr Christo Pantev; www.biomag.uni-muenster.de). Stimuli were delivered in blocks of 10s interleaved with 20s of rest, for a total of 10 blocks of stimulation and 10 blocks of rest. The first 8 s (4 TRs) of data acquired from each run were discarded to allow for fMRI signal equilibration. Subjects were instructed to keep their eyes closed throughout scanning and focus on the stimuli. A whole brain three dimensional (3D) high-resolution anatomical scan (124 sagittal slices, 24 x 24 cm FOV, 256 x� 256 matrix, 1.5 x 0.94 x 0.94 mm voxels) was acquired with a T1-weighted 3D spoiled gradient echo sequence (one signal average, flip angle = 20? , TE ?5 ms). In addition, two diffusion tensor imaging scans (38 axial slices, FOV 24 x 24 cm, 128 x 128 matrix, 1.875 x 1.875 x 3 mm voxels) were acquired along 23 directions with a b-value of 1000smm�2. Each run also contained two volumes with no diffusion weighting.

fMRI Analysis

Data were analysed using Brainvoyager QX v1.8 (Brain Innovaton, Maastricht, Netherlands). Pre-processing included: 3D motion correction, slice scan-time correction, linear trend removal, high-pass filtering (five cycles per run), and spatial smoothing with a 6mm full width at half maximum (FWHM) Gaussian kernel. fMRI data sets were interpolated to 3 x 3 x 3 mm voxels, registered to the high-resolution ana- tomical image, and normalized to standard Talairach space (Talairach and Tournoux, 1988). Voxels are reported as 1 x 1 x 1 mm. Data were analysed using the general linear model; the model was obtained by convolving the boxcar function of the time course of tactile stimulation with the standard haemodynamic response function. To identify between group differences in activation patterns a fixed effects analysis was performed with the contrasts: (i) healthy controls: stimulation 4 rest; (ii) PNIr: stimulation 4 rest; and (iii) healthy controls 4 PNIr. Activation maps were thresholded at a corrected value of P50.05 (derived from an uncorrected P50.0001 and 120mm3 contiguous voxels as previously reported: Taylor and Davis, 2009); this was also validated by running a Monte Carlo Simulation with AlphaSim application implemented in the Analysis of Functional Neuroimage (AFNI) software. This analysis included only the 11 patients that sustained transection of the right median nerve (n=9) or the right median and ulnar nerve (n = 2) (i.e. the three patients with a pure right ulnar nerve transection were not included in this analysis).

Cortical Thickness Analysis

Cortical thickness analysis was performed using Freesurfer (http:// surfer.nmr.mgh.harvard.edu); methods have been outlined in detail elsewhere (Dale et al., 1999; Fischl et al., 1999a, b; Fischl and Dale 2000). Briefly, high-resolution T1-weighted anatomical data sets were registered to the Talairach atlas (Talairach and Tournoux, 1988). This was followed by intensity normalization, skull stripping and separation of the hemispheres. Subsequently, the white/grey matter (called the white surface) and grey/CSF (called the pial surface) boundaries were identified and segmented. The distance between the white and pial surfaces was then calculated at every point in each hemisphere of the brain. To identify group differences between the 14 patients and 14 age/sex-matched controls, a general linear model analysis was performed at every point on the brain. As individual�s cortical topography is inherently heterogeneous, a 5mm FWHM spatial smoothing kernel was applied prior to statistical analysis. Data are displayed at a corrected P50.05 (derived from an uncorrected P50.0075 and 102 contiguous vertices); this was calculated by running a Monte Carlo simulation with AlphaSim. A vertex represents a point on a two dimensional sheet, and, in this study, the distance between two vertices is 0.80mm2.

As patients exhibited significant deficits in somatosensory function within the transected nerve territory, we hypothesized that measures of somatosensory function (vibration and touch detection) would correlate with cortical thickness in the contralesional post-central gyrus (primary and secondary somatosensory cortices). Therefore, we performed correlation analyses in the patient group between: (i) cortical thickness and vibration detection threshold; and (ii) cortical thickness and touch detection thresholds. One patient did not complete psychophysical assessment; therefore, this analysis included 13 PNIr patients. In addition, to determine if there was a relationship between cortical thickness and recovery time a correlation analysis was also performed between these two measures. These correlation analyses were restricted to the contralesional post-central gyrus by including a mask (taken from Freesurfer�s built in atlas) in the general linear model. A Monte Carlo simulation was performed that was restricted to the number of vertices within contralesional post-central gyrus; images are displayed with a corrected P50.05 (derived from an uncorrected P50.0075 and 68 contiguous vertices).

Diffusion Tensor Imaging Analysis

Diffusion tensor image processing was performed with DTiStudio (www.MriStudio.org) and FSLv.4.0 (www.fmrib.ox.ac.uk/fsl/). Images were first realigned with the Automatic Image Registration tool implemented in DTiStudio, using the first B0 image in the first series acquired as the template. This process corrects for subject motion and eddy-current distortion. All images were then inspected visually to assess image quality and the alignment of the separate diffusion tensor imaging runs. If an artefact was detected, the slice was removed prior to calculating the average of the two separate diffusion tensor imaging runs. Individual FA maps were calculated using the DTIFIT tool implemented in FSL. Voxel-wise statistical analysis was performed to identify group differences in the mean fractional anisotropy using Tract Based Spatial Statistics; for a full description of these methods see Smith et al. (2006). Briefly, images were non-linearly registered to a target image (MNI152), the mean image was then created from all datasets and this image was subsequently thinned to represent all tracts that were common to all subjects. Each subject�s highest fractional anisotropy values were then projected onto the skeleton by searching in white matter perpendicular to each point on the white matter skeleton. A whole-brain voxel-wise statistical analysis was then performed between groups (14PNIr and 14 healthy controls) and images were whole brain corrected at P50.05. In addition, a region of interest analysis was performed in white matter tracts adjacent to the contralateral S1, thalamus and bilateral anterior and posterior insula. These regions were chosen as they have previously been implicated in aspects of somatosensation and because they correspond with regions that were identified in the fMRI and cortical thickness analysis (CTA) group analyses. Regions of interest were drawn on the white matter skeleton as follows: (i) The contralateral S1 region of interest originated medially at the junction between the white matter skeleton of the corona-radiata and the skeleton section feeding into the post- central gyrus; terminating at the end of the tract within a given slice.

In the z direction the region of interest extended from z=49 to 57; white matter tracts supplying the hand region. (ii) The contralateral thalamus region of interest was restricted to white matter tracks surrounding the posterior and medial thalamic nuclei (nuclei involved in somatosensory function), extending from z = �1 to 4. (iii) Insular regions of interest were drawn bilaterally within white matter adjacent to the anterior and posterior insula based on criteria previously published by our lab (Taylor et al., 2008b). The region of interest extended from z = 2 to 8. Fractional anisotropy values were extracted from each of these regions of interest and a multivariate analysis of variance (MANOVA) was performed using the Statistical Package for the Social Sciences v13.0 (SPSS Inc, Chicago), which included fractional anisotropy values for all six regions of interest.

Results

Table 1 provides demographic details for study participants. All 14 patients sustained a complete transection of the right median and/or ulnar nerve followed by microsurgical repair at least 1.5 years prior to study enrolment. The time from surgery to testing ranged from 1.5 to 8 years with a mean (?SD) of 4.8 ? 3 years. Patients and controls did not (34 ? 10 years both groups; t = 0.04; P = 0.97).

Psychophysics

Vibration thresholds were calculated from all three measurements since one-way repeated measures analysis of variance (ANOVA) indicated no significant differences between the three trials [F (25, 1)=0.227, P=0.64]. Vibration and mechanical detection thresh- olds were significantly impaired in PNIr patients compared to healthy controls (vibration: t = 4.77, P50.001, Fig. 3A; mechanical: t=3.10, P=0.005, Fig. 3D).

Nerve Conduction Testing

Amplitude and latency measures obtained from each patient�s contralesional nerves were classified as normal by an experienced neurologist at the Toronto Western Hospital EMG Clinic. Nine of the 14 patients completed nerve conduction testing. Table 2 displays the average increase/decrease latency and amplitude data for sensory nerve conduction from the wrist to the abductor pollicis brevis (median) or abductor digiti minimi (ulnar) muscles and for sensory conduction from the wrist to D2 (median) and D5 (ulnar) compared to each patients uninjured contralesional nerve. Out of nine, seven patients had transections that included the median nerve. Of these seven, one patient had no detectable response during motor testing and another patient had no detectable response during sensory testing.

nerve el paso tx. In the six patients with detectable responses, motor conduction latencies were increased by 43% (t=6.2; P=0.002) and amplitudes were decreased by 38% (t=�2.6; P=0.045) when each patient�s transected nerve was compared to their non-injured side. Sensory conduction in median nerves also revealed a 26% increase in latency (t=3.9; P=0.011) and a 73% decrease in amplitude (t=�8.0; P=0.000) compared to normal contralesional nerves. In the four patients with ulnar nerve transections one patient had no detectable response during sensory nerve testing. In those patients with responses, ulnar nerve motor latencies were not significantly elevated (t = 2.8; P = 0.070); however, amplitudes were significantly
decreased by 41% (t = �5.9; P = 0.010). Sensory testing of the ulnar nerve demonstrated a 27% increase in latency (t = 4.3; P = 0.049) but no significant increase in amplitude (t = 3.5; P = 0.072).

Functional Plasticity In The Primary Somatosensory Cortex

Functional MRI maps were calculated from the 11 PNIr patients with right median nerve transections (patients with ulnar nerve transections were excluded from this analysis) and 11 age- and sex-matched healthy controls. From Fig. 1A, it is clear that PNIr patients have significantly less activation, compared to healthy controls, in a region of S1 corresponding to Brodmann area 2 (BA2) (Talairach and Tournoux, 1988) and S2 (see Table 3 for details). The average event-related responses from these regions of interest highlight the attenuated BOLD response within the patients� left BA2 and left S2 (Fig. 1B and C, respec- tively). Curiously, vibrotactile stimulation in the patients activated a more superior part of the post-central gyrus (probably BA1/3) (Talairach and Tournoux, 1988) (Fig. 1A and Table 3). An event- related average (Fig. 1D) demonstrates that healthy controls had minimal activation in this region. Furthermore, patients had significantly more activation in brain regions collectively known as the task positive network (asterisks in Fig. 1). See Table 3 for the full list of task positive brain areas activated. This network includes lateral prefrontal, lateral parietal, premotor and inferior temporal cortices (Table 3): brain areas that are activated during the performance of an attention demanding task and suppressed or inactive during rest or tasks that are not cognitively or attentionally challenging (Fox et al., 2005; DeLuca et al., 2006; Seminowicz and Davis 2007).

Reduced Grey Matter In The Primary Somatosensory Cortex Correlates With Sensory Recovery

Cortical thickness analysis in all 14 patients and 14 age/ sex-matched healthy controls revealed several loci of significant cortical thinning in the PNIr group (Fig. 2 and Table 4). Specifically, patients had a 13%�22% reduction in cortical thick- ness in the left (contralesional) S1, S2, pregenual anterior cingulate gyrus, ventrolateral prefrontal cortex and right anterior insula, anterior/posterior mid cingulate gyrus and paracentral lobule. Interestingly, the locations of grey matter thinning within the post-central gyrus coincide with the regions of reduced BOLD following vibrotactile stimulation (Table 4). Since we had prior knowledge of the patients� sensory deficits and recovery time (i.e. time since microsurgical repair), we next asked whether the patients� cortical thickness in the post-central gyrus correlated with their sensory mechanical and vibration detection thresholds, or with their recovery time. These analyses revealed a negative correlation between cortical thickness and vibration detection thresholds in a region encompassing BA1/2 and S2 (P50.001, r=?0.80 and ?0.91, for BA1/2 and S2, respectively; Fig. 3 and Table 5). In addition, mechanical detection thresholds were also negatively correlated with cortical thickness in a slightly more superior BA2 region and the same S2 region (P50.001, r = ?0.83 and ?0.85, for BA2 and S2, respectively; Fig. 3 and Table 5). However, we did not identify a significant relationship between recovery time and cortical thickness. Therefore, in the post-central gyrus cortical thinning was associated with more severe sensory deficits. However, we did not identify a significant relationship between recovery time and cortical thickness. Again, there was a correspondence between the cortical thinning in areas negatively correlated with vibratory stimuli and the regions showing group fMRI and CTA abnormalities.

White Matter Abnormalities Following Nerve Transection

To assess white matter integrity we utilized a region of interest approach to examine white matter group differences based on a priori hypotheses. Regions of interest were restricted to white matter tracts surrounding and feeding into the contralesional S1 and thalamus. In addition, we also drew regions of interest in white matter adjacent to left and right, anterior and posterior insula. The insula was chosen as it is implicated in somatosensory processing and because we identified reduced grey matter in the right anterior insular with CTA. This region of interest approach revealed that patients had significantly reduced white matter fractional anisotropy values (MANOVA including all six regions of interest) adjacent to the right anterior [F (1, 26) = 4.39, P = 0.046; Fig. 4A] and posterior insula [F (1, 26) = 5.55, P = 0.026; Fig. 4B], but there were no group differences in the white matter adjacent to the left insula (left anterior insula: P = 0.51; left posterior insula: P=0.26), thalamus (P=0.46) or S1 (P=0.46).

nerve el paso tx.Discussion

Here, we have demonstrated for the first time that there is functional plasticity and both grey and white matter structural abnormalities in several cortical areas following upper limb peripheral nerve transection and surgical repair. This plasticity may arise from incomplete peripheral nerve regeneration (peripheral cell death and/or incomplete re-myelination), as nerve conduction measures in these patients demonstrated severe abnormalities. In addition, our data demonstrate that decreased vibrotactile-evoked fMRI responses in the post-central gyrus correspond with grey matter thinning in the patient group. These results suggest that reduced BOLD responses may be facilitated by a reduction in cortical grey matter and/or a decrease in the afferent input to the post-central gyrus. In addition, cortical thickness within these same parts of the post-central gyrus negatively correlated with behavioral measures of somatosensory function. That is, increased somatosensory deficits were correlated with thinner cortex; both of which may be related to afferent input. Taken together, our data suggest that incomplete peripheral nerve regeneration contributes to somatosensory impairments, cortical grey matter atrophy and reduced fMRI activation (see Fig. 5 for a summary of these findings).

It is well known that cortical plasticity following peripheral nerve transection and surgical repair can occur throughout the CNS in non-human primates (Kaas, 1991). This plasticity is thought to be due to the unmasking of previously silent synapses or axonal sprouting into deafferented territory (Wall et al., 1986; Florence and Kaas, 1995). In the primate model, 1 year following nerve transection and surgical repair, the denervated cortex is characterized by incomplete and disorderly representations of the regenerated and adjacent (intact) nerves. This patchy representation is attributed to incomplete peripheral regeneration resulting in a partial recovery of the denervated cortical space (Kaas, 1991). To assess the extent of peripheral regeneration in our patient population we performed sensory and motor nerve conduction studies across the transected area. Our nerve conduction results demonstrate that PNIr patients have significantly decreased amplitude and increased latency in both sensory and motor nerves compared to their own untransected side. Decreased amplitude combined with increased latency is indicative of peripheral fibre loss (i.e. cell death) and/or abnormal or incomplete re-myelination following transection (Kimura, 1984). In addition, it is well established that between 20% and 50% of dorsal root ganglion neurons die following nerve transection (Liss et al., 1996). Thus, afferent cell death and incomplete regeneration can result in decreased afferent input to the cortex, which may account for ongoing sensory deficits and decreased BOLD response in BA2 and S2. Furthermore, this diminished afferent input could also account for the cortical thinning we observed in the same regions of the cortex. Sensory deprivation has been shown to cause trans- neuronal degeneration in several regions of the CNS, including the dorsal horn following sciatic nerve section (Knyihar-Csillik et al., 1989), and may involve second- and third-order neurons (Powell and Erulkar, 1962). Transneuronal degeneration is characterized by cell shrinkage and is thought to be related to decreased, or non-existent, afferent input (Knyihar-Csillik et al., 1989). Thus, cortical grey matter loss (or atrophy) could also be directly related to decreased afferent input.

nerve el paso tx.

nerve el paso tx.

nerve el paso tx.

nerve el paso tx.We also demonstrated increased activation in the post-central gyrus in a region corresponding to BA1/3 (Talairach and Tournoux, 1988). Electrophysiological, anatomical tracing and neuroimaging studies have established that for the majority of cutaneous mechanoreceptive afferents the first cortical destina- tions are BA1 and BA3b. These cytoarchitectonic brain areas each possess a somatotopic body map with small receptive fields. In addition, these areas respond to many features of tactile information, such as texture and roughness, velocity and curvature of stimuli (Bodegard et al., 2001). fMRI studies have demon- strated that activity within the somatosensory cortex is influenced by attention such that fMRI responses to tactile stimuli in S1 are increased when subjects attend to a tactile stimulus, but are atte- nuated when subjects are distracted (Arthurs et al., 2004; Porro et al., 2004). Furthermore, our patients activated a network of brain areas known as the task positive network (DeLuca et al., 2006) more than healthy controls. These brain areas are activated during attention demanding processes (Fox et al., 2005; Seminowicz and Davis, 2007). Together, these findings imply that patients must attend to the stimulus more than controls because of their impaired sensory input. This increased attention may also account for the increased activation in BA1/3b. Of course, the increased activation in BA1/3b may also reflect plasticity that is unrelated to attentional load.

nerve el paso tx.

nerve el paso tx.

nerve el paso tx.BA2 and S2 both receive projections from BA1/3b and also from distinct parts of the ventroposterior thalamic complex (Pons et al., 1985; Friedman and Murray, 1986). Both of these brain areas have large, often multi-digit (BA2) or bilateral (S2) receptive fields (Pons et al., 1985; Iwamura et al., 2002). Based on ana- tomical projections and neuronal response properties, hierarchical processing of tactile information has been demonstrated from BA1/3b to BA 2 (Kaas et al., 2002). In addition, electrophysiolo- gical studies in macaques (Pons et al., 1987) and magnetoence- phalography data acquired in humans, suggest that serial processing of tactile inputs occurs from S1 to S2 in higher primates (Frot and Mauguiere 1999; Disbrow et al., 2001). Several studies have demonstrated that BA2 is preferentially activated by shape and curvature (Bodegard et al., 2001), while S2 may be involved in tactile learning (Ridley and Ettlinger 1976; Murray and Mishkin, 1984), supporting the notion that these brain areas are involved in higher-order somatosensory processing. Our psychophysical assessment demonstrated that patients were significantly impaired at the detection of simple tactile stimuli, and in the Shape Texture Identification test 1.5 years after surgery (Taylor et al., 2008a). This latter test assesses a patient�s ability to recognize character- istics of an object while actively exploring a shape or texture, requiring the integration of sensory information across regions of the body (Rosen and Lundborg, 1998). Taken together, one inter- pretation of our data is that PNIr patients attend more to the vibrotactile stimulus, leading to increased activation of the task positive network and BA1/3. However, in these patients, our data imply that higher-order processing areas, such as BA2 and S2, did not receive tactile information, which, in turn, may result in cortical thinning and reduced BOLD responses.

The insula is thought to play a role in integrating multimodal information important for sensorimotor, emotional, allostatic/ homeostatic and cognitive functions (Devinsky et al., 1995; Critchley, 2004; Craig, 2008) and has been designated a limbic sensory cortex (Craig, 2008). Several studies have reported insular activation in response to tactile stimulation (Gelnar et al., 1998;

Downar et al., 2002) and anatomical tracing studies in primates have demonstrated that the insula is reciprocally connected to frontal, parietal and temporal lobes (Augustine, 1996). In our patients, the right anterior insula was the only cortical area that demonstrated significant cortical thinning in conjunction with reduced fractional anisotropy values in the adjacent white matter, suggesting that the cortical thinning within this region is associated with a loss of fibres projecting to or from this structure. The right anterior insula has been implicated in interoception as it is situated to integrate homeostatic input from the body with motivational, emotional and social conditions (Craig, 2008). Furthermore, Critchley et al. (2004) reported a correlation between interoceptive abilities and the grey matter volume of the right anterior insula. Given our finding that the patients have decreased grey matter in the right anterior insula, it would be of interest to assess interoceptive capabilities following peripheral nerve injury in a future study.

Taken together, we have demonstrated for the first time that functional and structural alterations are present in the human cerebral cortex 1.5 years after a complete transection of an upper limb peripheral nerve that was microsurgically repaired. In addition, nerve conduction measures indicate incomplete peripheral regeneration in these patients. Furthermore, we show that cortical thickness is related to psychophysical measures of recovery, in that thinner cortex within BA2 and S2 was associated with poorer somatosensory function. These data suggest that the reestablishment of normal functional activation maps is directly associated with the successful regeneration of peripheral afferents.

Keri S. Taylor,1,2 Dimitri J. Anastakis2,3,4 and Karen D. Davis1,2,3

1 Division of Brain, Imaging and Behaviour � Systems Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, Canada M5T258
2 Institute of Medical Science, University of Toronto, Canada
3 Department of Surgery, University of Toronto, Canada
4 Clinical Studies Resource Centre, Toronto Western Research Institute, University Health Network, Toronto, Canada M5T2S8

Correspondence to: Karen D. Davis, Ph.D.,
Division of Brain, Imaging and Behaviour � Systems Neuroscience, Toronto Western Research Institute,
Toronto Western Hospital,
University Health Network,
Room MP14-306, 399 Bathurst Street,
Toronto, Ontario,
Canada M5T 2S8
E-mail: kdavis@uhnres.utoronto.ca

Acknowledgements

The authors thank Mr. Geoff Pope, Dr. Adrian Crawley, Mr. Eugene Hlasny and Mr. Keith Ta for expert technical assistance. The authors would like to thank Dr. Peter Ashby and Mr. Freddy Paiz from the Toronto Western Hospital EMG Clinic for conduct- ing the nerve conduction tests and for providing expert assess- ment of the findings. The authors also thank Drs Dvali, Binhammer, Fialkov and Antonyshyn for collaborating with this project. Dr. Davis is a Canada Research Chair in Brain and Behaviour (CIHR MOP 53304).

Funding

The Physicians� Services Incorporated and a joint seed grant from the University of Toronto Centre for the Study of Pain/ AstraZeneca.

Supplementary material

Supplementary material is available at Brain online.

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Close Accordion
Epigenetic Influences On Brain Development And Plasticity

Epigenetic Influences On Brain Development And Plasticity

Epigenetic: A fine interplay exists between sensory experience and innate genetic programs leading to the sculpting of neuronal circuits during early brain development. Recent evidence suggests that the dynamic regulation of gene expression through epigenetic mechanisms is at the interface between environmental stimuli and long lasting molecular, cellular and complex behavioral phenotypes acquired during periods of developmental plasticity. Understanding these mechanisms may give insight into the formation of critical periods and provide new strategies for increasing plasticity and adaptive change in adulthood.

Introduction

During early development, neuronal circuits are created and connections between neurons undergo remodeling as they develop their adult functional properties in response to the surrounding environment. The adult brain loses this extraordinary plasticity. Recent findings support a key role of epigenetic factors in mediating the effects of sensory experience on site-specific gene expression, synaptic transmission, and behavioral phenotypes. Here we review recent evidence implicating multiple epigenetic mechanisms in experience-dependent changes during development and discuss their role in critical period expression in the developing and adult brain.

Epigenetics: Molecular Mechanisms Of Gene Regulation

The term �epigenetic� refers to chromatin modifications which alter gene expression without affecting DNA sequence. The factors that contribute to the epigenetic regulation of transcriptional activity are numerous and include microRNA [1], DNA methylation [2,3] and post- translational modifications of nucleosomal histones [2,4]. DNA methylation refers to a chemical modification to DNA whereby cytosine is converted to 5-methylcytosine with the consequence of reduced accessibility of the DNA to transcription factors (Figure 1a�d). These modi- fications can be stable and heritable and provide a critical mechanism in cellular differentiation [3]. The process of methylation is dependent on the presence of methyl donors (provided by nutrients such as folic acid, meth- ionine and choline) and methyltransferases which med- iate either maintenance (i.e. DNMT1) or de novo DNA methylation (i.e. DNMT3). Transcriptional repression associated with DNA methylation is further sustained through methyl-binding proteins such as MeCP2 [5]. Epigenetic control of gene expression is also mediated through multiple post-translational modifications of histone proteins, including methylation, acetylation and ubiquination, which can alter the accessibility of DNA and the density of chromatin structure (Figure 1e,f). In particular, histone acetylation is associated with increased transcriptional activity whereas histone deacetylation is associated with transcriptional repression. The acetylation state of these nucleosomal proteins is controlled by the presence of histone acetyltransferases (HATs), histone deacetylases (HDACs), which are recruited by methyl-binding proteins, and by HDAC inhibitors, which effectively increase gene expression through shifting histones to an acetylated state [2,6]. The timing and degree of gene expression are controlled through these complex mechanisms, thus providing a link between single genotypes and multiple phenotypes.

Epigenetic Factors & The Influence Of Early Life Experiences

In mammalian development, the prenatal and postnatal periods are characterized by rapid changes in neuronal organization, thus providing a critical window of opportunity during which environmental experiences can lead to long-term influences on brain and behavior. There is increasing evidence for the role of epigenetic factors in mediating the relationship between these experiences and long-term outcomes. Mueller and Bale [7] have recently demonstrated decreased DNA methylation of the corticotrophin-releasing-factor (CRF) gene promotor and increased methylation of the glucocorticoid receptor (GR) exon 17 promotor region in hypothalamic tissue of adult male mice born to gestationally stressed females. These epigenetic modifications are associated with exposure to stress during the early stages of prenatal development and may involve dysregulation of placental gene expression. The nutritional environment during fetal development has likewise been demonstrated to influence growth, metabolism and brain development and there is increasing evidence that dietary levels of methyl-donors can epigenetically alter gene expression in offspring [8,9]. In rats, Lillycrop et al. [10] illustrate that GR 110 and PPARa (peroxisome proliferator-activated receptor alpha) gene promotor methylation is reduced in the hepatic tissue of offspring born to protein restricted dams whereas methylation is increased in offspring of dams whose diet is supplemented with methyl donors [10,11]. These effects may be related to DNMT1 expression, which is likewise decreased with dietary protein restriction [11]. Prenatal nutritional regulation of DNA methylation has similarly been observed in brain tissue associated with levels of DNMT1 expression [12], suggesting that in the rapid period of cell division ocurring during fetal development, the level of methyl donors can have a significant impact on transcriptional activity that is maintained into adulthood.

epigenetic el paso tx.

The role of epigenetic modification in sustaining the effects of environmental experience has also been demonstrated in the context of postnatal mother�infant interactions. Individual variations in maternal care during the immediate postpartum period in rats are associated with changes in offspring hypothalamic-pituitary-adrenal (HPA) activity, neuroendocrine systems involved in reproduction and hippocampal plasticity [13]. Analyses of levels of promotor methylation within the hippocampal GR 17 and hypothalamic ERa genes in offspring of rat dams that provide high vs. low levels of maternal care indicate that high levels of care are associated with decreased promotor methylation and thus increased gene expression [14,15]. Though the route through which these epigenetic changes are mediated is not yet clear, there is evidence for increased binding of nerve growth factor-inducible protein A (NGFI-A) to the GR exon 17 promoter amongst offspring who receive high levels of care in infancy [15] and in vitro models suggest that NGFI-A up-regulation is associated with histone acetylation, DNA demethylation, and activation of the exon 17 GR promoter [16]. The relevance of these effects in humans has recently been demonstrated by Oberlander et al. [17] in the analysis of methylation status of the GR promotor at NGFI-A binding sites in cord blood mononuclear cells of infants exposed to third trimester maternal depressed or anxious mood. Maternal depression was found to be associated with increased GR 1F promotor methylation in fetal blood samples and these methylation patterns predicted HPA reactivity in infants at 3 months of age [17]. Analysis of hippocampal tissue from suicide victims with a history of childhood abuse similarly indicates lower GR expression and higher GR 1F promotor methylation associated with disruptions of the early environment and confirms the findings from rodent studies that differential NGFI-A binding is a functional consequence of these epigenetic effects [18]. However, the impact of perinatal mother� infant interactions is not limited to GR regulation as illustrated by Roth et al. [19] examining the effects of postnatal abuse on offspring brain derived neurotrophic factor (BDNF) methylation [19]. In rats, an increase in methylation of exon IV of the BDNF promotor and consequent decrease in BDNF mRNA in the prefrontal cortex was found in association with exposure to periods of abusive maternal care (dragging, rough handling, etc.). As was the case with the effects of individual differences in maternal care, these effects emerged in infancy and were sustained into adulthood. Moreover, these effects on BDNF exon IV methylation are perpetuated to the F1 generation suggesting a role for epigenetic mechanisms in transgenerational effects [20].

Development Across The Lifespan: Epigenetics & Experience Dependent Plasticity

The previous section highlights the stable effects of early life experiences and how these events become encoded at a molecular level. Another approach to the study of epigenetics and development comes from studies of synaptic plasticity during the expression of long-term potentiation (LTP) and memory consolidation. High levels of maternal care and exposure to juvenile environ- mental enrichment (EE) have been demonstrated to improve capacity for learning and memory associated with LTP enhancement [21,22]. Moreover, recent evidence suggests that EE modulates NMDAr/p38/LTP signaling pathways in the hippocampus and improves contextual fear memory formation across generations such that offspring of enriched mothers likewise show enhanced LTP even when cross-fostered at birth to non- enriched mothers [23]. Environmental enrichment has been associated with increased histone acetylation in the hippocampus and improved spatial memory [24,25]. Pharmacological targeting of the epigenome has been used to demonstrate the role of histone acetylation and DNA methylation in the consolidation of long-term memory [26]. Treatment with zebularine (an inhibitor or DNA methyltransferases) has been shown to block memory formation and reduce histone acetylation following con- textual fear conditioning in adult rats [27] whereas treatment with the HDAC inhibitor sodium butyrate lead to enhanced formation of contextual fear memories [28]. The particular HDAC target of these inhibitors may be HDAC2 as recent evidence has emerged illustrating decreased synaptic plasticity and memory formation in mice over-expressing HDAC2 but not HDAC1; with the converse effect in HDAC2-deficient mice [29]. These studies illustrate a possible relationship between synaptic activity and histone acetylation/DNA methylation in mature neurons, suggesting that there is continued plasticity in these epigenetic systems beyond the prenatal and postnatal periods of development.

Epigenetic Mechanism & The Regulation Of Synaptic Transmission

Activity-dependent changes in gene expression within neuronal pathways during development may serve as a critical pathway linking experience of the external environment and epigenetic modifications within the cell nucleus. In a recent study, Monteggia and colleagues elegantly demonstrated that spontaneous synaptic trans- mission in hippocampal neurons is regulated by alterations in DNA methylation that occur in response to synaptic activity [30]. Treatment with a DNMT inhibitor lead to a significant decrease in frequency of miniature excitatory post-synaptic currents (mEPSCs) and rate of spontaneous synaptic vesicle fusion correlated with a decrease in BDNF promoter I methylation and increased BDNF expression. This effect was blocked with inhibition of synaptic activity and reductions in mEPSCs were prevented in the absence of MeCP2. These results strongly suggest a role for DNA methylation/MeCP2 pathways in the control of synaptic function. Activity- dependent phosphorylation of MeCP2 via Ca2+-calmodulindependent kinase II has been shown to cause MeCP2 dissociation from target genes and relieve transcriptional repression [31]. Consequently, genes such as BDNF are increased in expression leading to normal dendritic patterning and dendritic spine development [32]. These findings suggest an epigenetic mechanism through which neurons can monitor alterations in activity level and adjust neurotransmitter output via altered gene expression with consequences for network excitability and circuit refinement. Impairments in these MeCP2 pathways may lead to several neurodevelopmental abnormalities including Rett syndrome, infantile autism, mental retardation, and schizophrenia [33] and targeted deletion of MeCP2 in the amygdala has recently been demonstrated to impair learning and memory and lead to increased anxiety-like behavior in mice [34].

Epigenetic Control Of Critical Period Plasticity

Though epigenetic mechanisms have certainly been implicated in mediating the high levels of plasticity in early development, it is also possible to view the decreased plasticity and sensitivity that occurs later in development from an epigenetic perspective. Neocortical circuits are extremely sensitive to manipulations of the sensory environment during restricted temporal windows of postnatal development called �critical periods�. For example, an imbalance in binocular vision during child- hood affects perception leading to amblyopia or �lazy eye�. Monocular deprivation (MD) reproduces this classical paradigm of experience-dependent plasticity [35]. The striking physiological effect of MD is a shift in visual cortical neuron response in favor of the non-deprived eye; an example of ocular dominance (OD) plasticity. The critical period during which this OD plasticity occurs is defined by the activation and subsequent inhibition of specific molecular pathways involving signaling molecules such as aCaMKII, calcineurin, PKA, ERK, and CREB [36]. Recently, Pizzorusso and colleagues identified rapid increases in ERK-dependent phosphorylation of histones associated with activation of the juvenile visual cortex and a developmental downregulation of this effect in older mice [37]. In adult mice, the reduced OD plasticity can be reinstated through treatment with the HDAC inhibitor trichostatin A (TSA). Multiple cellular mechanisms might contribute to experience-dependent plasticity expression [38]. Further work is necessary to understand if epigenetic mechanisms are generally acting in all cellular substrates or only within a specific subset.

Myelin maturation has also been proposed as one of the major factors contributing to decreased neuronal plasticity. During the onset of critical period plasticity, oligodendrocytes start to express specific myelin structural proteins, including myelin basic protein (MBP), myelin-associated glycoprotein (MAG), myelin oligodendrocyte glycoprotein (OMgp) and myelin-associated oligodendrocyte basic protein (MOBP) [39]. As myelination reaches adult levels, OD plasticity is strongly reduced or absent. MAG and OMgp may contribute to critical period closure through activation of Nogo receptors. Indeed, mice lacking Nogo receptors exhibit OD plasticity even in adulthood [40]. Manipulation of epigenetic status of oligodendrocytes may also be an effective strategy for modulating plasticity. Casaccia-Bonnefil and colleagues have shown that histone modifications are involved in oligodendrocyte precursor cell (OPC) differentiation during development and in recovery from injury [41� 43]. Administration of the HDAC inhibitor valproic acid during the critical period of myelination onset was found to prevent the OPC maturation into myelinating cells. These results suggest that HDAC activity during a specific temporal window of postnatal development is required for OPC differentiation and myelination. At later developmental stages, histone deacetylation subsides and is replaced by repressive histone methylation and the establishment of a compact chromatin structure, characteristic of the differentiated oligodendrocyte phenotype [43]. Shen et al. [44] found that in response to damage of oligodendrocytes, robust remyelination occurred in juvenile but not in older animals with the new myelin synthesis preceded by down regulation of oligodendrocyte differentiation inhibitors and neural stem cell markers and the recruitment of HDACs to promoter regions. This HDAC recruitment is inefficient in older brains, allowing for the accumulation of transcriptional inhibitors and prevention of myelin gene expression. This age-depend- ent effect can be induced in young mice treated with HDAC inhibitors during the period when damage to oligodentrocytes is occurring. Thus, there are epigenetic changes that are characteristic of periods of developmental plasticity that could provide a target for therapeutic intervention in the event of CNS damage. The use of HDAC inhibitors to increase plasticity in the brain may be a promising therapeutic approach as there is conver- ging evidence from rodent models that treatment with these compounds (1) can lead to dramatic shifts in gene expression and behavior in adult offspring who have received low levels of maternal care [15] and (2) mimic the effects of EE on reversal of neurodevelopmental abnormalities [24]. Rather than producing a generalized increase in transcription, these compounds lead to acti- vation of a specific subset of genes [45�47], suggesting possible targeted intervention to reinstate plasticity in adult brain.

Conclusions

There is converging evidence for the role of epigenetic modifications such as histone acetylation and DNA meth- ylation in both the stability and plasticity of developing neuronal circuits. The persistent effects on gene expression that can be achieved through these mechanisms provide a biological route through which environmental experiences can become embedded, leading to long-term changes in neurobiology and behavior. Enhancing plasticity in the adult brain is an exciting prospect and there is certainly evidence emerging that suggest the possible use of epigenetic factors to induce a �younger� brain. The challenge of future studies is to establish the pathways through which site-specific and gene-specific transcriptional modifications can be achieved and to better understand the route through which experiences across the lifespan induce this molecular plasticity.

Michela Fagiolini 1, Catherine L Jensen 2 and Frances A Champagne 2

Current Opinion in Neurobiology 2009, 19:1�6
This review comes from a themed issue on Development
Edited by Takao Hensch and Andrea Brand
0959-4388/$ � see front matter Published by Elsevier Ltd.
DOI 10.1016/j.conb.2009.05.009

Corresponding author: Champagne, Frances A (fac2105@columbia.edu)

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