neuropathy - Padda Institute Center for Interventional Pain Management

Diabetes and Neuropathy

Diabetic Peripheral Neuropathy (DPN) is the most common complication of diabetes, and often presents as a distal, symmetric, sensorimotor neuropathy. In the United States, 26.8 million people are affected by diabetes; by the year 2030, that number is predicted to increase to approximately 35.9 million people.

In the U.S. alone, the annual total direct medical and treatment costs of diabetes were an estimated $44 billion in 1997, representing 5.8 percent of total personal healthcare expenditures during that year. When it comes to diabetic peripheral neuropathy and its complications, management is resource intensive and long-term, accounting for a large proportion of this total expenditure. In 2001, the total annual cost of diabetic peripheral neuropathy and its complications in the U.S. was estimated to be between $4.6 and $13.7 billion. Up to 27 percent of the direct medical cost of diabetes may be attributed to diabetic peripheral neuropathy.

More than half of patients who have type 1 or 2 diabetes develop DPN. Diabetes is associated with both macrovascular and microvascular complications, in which the major microvascular complication is diabetic neuropathy (DN) with a prevalence of 50–60%. The neuropathy progresses with decreasing nerve functionality and nerve blood perfusion which may result in malnourished nerve and leads to permanent nerve damage. The clinical manifestations of diabetic neuropathy include numbness, burning and tingling sensation, and intractable pain.

 

Many patients with neuropathy simply don’t now they have it

You may have nerve damage well before you experience its symptoms. The first time you may notice diabetic nerve pain symptoms is when the nerve damage has already progressed. Neuropathy is known to develop well before the patient has any symptoms, and the literature states unequivocally that the sooner treatment can be initiated, the greater the chances of reversal of the symptoms. Microvascular circulatory deficiencies, caused by errors in glucose metabolism, for example, have direct effects on the circulation to the nerves, and there are direct effects on the nerves themselves. Pain signals, in turn, trigger secondary peripheral and central hyperalgesia which enhance the body’s response to the microvascular insult. On a local level, microinflammation and edema around the nerves also contribute to the neuropathy. While this nerve damage can cause pain, it can also result in a loss of feeling in the feet and hands. Numbness can cause cuts and foot ulcers to go unnoticed. These cuts can lead to an infection. In severe cases, an untreated infection can even result in amputation.

 

DPN affects the nerves in the hands and feet, causing numbness, tingling, and pain. Clinical symptoms associated with DPN involve poor gait and balance associated with large sensory fibers and abnormal cold and/or heat sensation associated with small sensory fibers. Chronic pain associated with diabetes is represented by hyperalgesia, allodynia, paresthesias, and spontaneous pain. Symptoms are described as tingling, “pins and needles,” burning, itching, and an abnormal sensation to pain and temperature. Over time, these symptoms may advance from the toes to the foot and up the leg, and these symptoms may occur in the fingers and hands.

Tingling and Numbness

Scientists aren’t sure exactly how diabetes damages nerves. Some theorize that the excess blood sugar affects the protective coating on nerves. Others believe decreased blood flow to the nerves can cause damage.

Either way, as the disease progresses, patients may feel a tingling or numbness in the fingers, toes, hands, and feet. Patients may also report a “pins and needles” feeling, or even a burning sensation.

 

Shooting Pain

A nerve that’s pinched or suffering from damage may send out signals that cause shooting pains. People also described this sensation as an electric shock, or a sharp, stabbing pain. The sensations usually come and go, but they may also remain more constant at times.

These types of pains are most common at night, and can disturb sleep. They may also be the result of damaged nerves that are sending out mistaken signals to the brain (misfiring).

 

Inability to Feel Hot and Cold

Our nerves help us to sense the world around us. They are how we notice when we’re feeling hot or cold. They also tell us when we’ve stubbed a toe or suffered a paper cut.

When nerves are severely damaged, they can actually die off. Suddenly, you may no longer be able to tell when you’ve stepped on a tack or suffered a blister. That means small injuries can go unnoticed and untreated. This can cause more problems down the road.

 

Foot Problems

Once a person loses function in some of the nerves in the feet, they may not notice a blister, infection, or wound until it becomes infected, swollen, and inflamed. Nerve damage can also lead to changes in the shape of the toes. This can require shoe-fitting adjustments. Doctors always recommend that people with diabetes check their feet and hands daily for injuries, especially those who’ve suffered nerve damage and lack feeling in the fingers or toes.

 

Difficulty Walking and Performing Other Daily Tasks

It’s because of our nerves we can button up a shirt, create a hairstyle for ourselves, or even open a doorknob. Nerve damage in the hands and feet can make these everyday tasks more difficult or even impossible. But there are tools available that can help. Specialized orthotic inserts, diabetic shoes, and gripping tools are just a few examples.

 

Autonomic Symptoms

Did you know that nerves control the digestive system? They are also involved in perspiration, sexual function, heart rate, urinary function, and more. If diabetes affects any of these nerves, patients may experience the following symptoms:

  • stomach upset (constipation, diarrhea, nausea, vomiting)
  • urinary problems (incontinence or urinary tract infections)
  • erectile dysfunction or vaginal dryness
  • inability to stay warm or cool
  • difficulty focusing your eyes
  • dry, cracked skin

 

Nerve Pain and Sleep

Some nerve pain is worse at night and as a result, the individual can have difficulty sleeping. This loss of sleep can cause additional problems so people with this type of nerve pain need to discuss the problem with their doctor to receive early treatment.

 

Coping with Nerve Damage

To avoid or limit any of these symptoms, concentrate on controlling your blood sugar levels. The more you can keep your levels in the normal range, the slower any nerve damage will progress. Exercise regularly, manage your weight, and take steps to reduce stress.

Talk to your doctor about lifestyle changes and tools that can help you cope once nerve damage has occurred. Medications and specific treatment methods are also available to help reduce symptoms. Your doctor is your partner in controlling nerve pain. By answering all questions asked (pain type, duration, and how it has changed your lifestyle), you help your doctor to determine the cause of the pain and how to treat it.

 

Treating diabetic nerve pain requires a specific treatment:

Diabetic nerve pain, or painful diabetic peripheral neuropathy, is a separate condition from diabetes that is caused by high blood sugar related to diabetes. This nerve damage may cause foot pain and hand pain. If you suffer from diabetic nerve pain, you can’t undo the damage that has already occurred but it’s very important that you don’t ignore your pain either. The pain, which may get worse over time, can be treated.

Control of your blood sugar

If you have diabetes, it is important to control your blood sugar. Your doctor has probably tested your A1C level before. This measures your average blood sugar level over the past 3 months. The American Diabetes Association recommends a goal of 7% or lower.

Do something about your diabetic nerve pain

Controlling your blood sugar can prevent further nerve damage. However, that won’t reverse the damage or relieve your diabetic nerve pain. And since nerve pain isn’t like other kinds of pain, you may need to receive a specific diabetic nerve pain treatment.

 

What treatment options are available for diabetic nerve pain?

The most common approach is oral medications that only mask the symptoms.

  • 50 percent of patients with diabetic peripheral neuropathy receive treatment with opioids
  • 40 percent take anti-inflammatory drugs
  • 20 percent use serotonin selective reuptake inhibitors (SSRI)
  • 11 percent take tricyclic inhibitors
  • 11 percent take anticonvulsants (Neurontin and Lyrica).

 

Although there is a range of pharmacological agents available for treating the pain associated with diabetic neuropathy, only duloxetine and pregabalin are approved by US Food and Drug Administration (US FDA) for the treatment of diabetic neuropathic pain. The “gold standard” in treating peripheral neuropathy, pregabalin (Lyrica, Pfizer), helps 39 percent of patients achieve a 50 percent reduction in their discomfort and pain, but causes at least 38 percent to have complications. These medications have drawbacks and major adverse effects.

 

Over-the-counter pain relief pills are not approved by the FDA to treat this specific pain. Diabetic nerve pain is a form of nerve pain, a unique type of pain that is different than other types of pain, like pain from a headache, muscle ache, arthritis or sprained ankle. Over-the-counter pain relief pills are not approved by the FDA for the treatment of diabetic nerve pain.

 

What is Combined Therapy?

Combined therapy incorporates two well established procedures that have been combined into a protocol that is showing great promise as an effective treatment solution for diabetic and idiopathic neuropathies. Combined therapy consists of two procedures, an ankle block performed with local anesthetic, and Electronic Signal Treatment (EST), as delivered by a unique sophisticated electroanesthetic wave generator.

 

Ankle Block

The ankle block targets five nerves responsible for sensory supply distal to the ankle. The nerves consist of four branches of the sciatic nerve (the superficial peroneal, the deep peroneal, the sural, and the posterior tibial nerve) and one cutaneous branch of the femoral nerve (the saphenous nerve). The sciatic nerve gives off two terminal branches, the common peroneal and the tibial nerve.

 

Electronic signal treatment

EST is an electrical signal wave treatment that regenerates nerves and increases blood flow by using electrical waves to simulate nerve function in the damaged areas. Electronic signal treatment utilizes computer-controlled, exogenously delivered specific parameter electronic cell signals using both varied amplitudes (AM) and frequencies (FM) of electronic signals. This

digitally produced electronic sinusoidal alternating current with associated harmonics produces scientifically documented and/or theoretical physiological effects when one applies them to the human body. The electronic signal treatment medical device uses sophisticated communications technology to produce and deliver higher frequency signal energy in a continually varying sequential and random pattern via specialty electrodes. This alternation of sequential and random electronic signal delivery eliminates neuron accommodation.

With the help of 0.25% Marcaine, which is a vasodilator (opens the blood vessels for a short time to increase blood flow) and a local anesthetic. The more blood flow that your nerves get while stimulated the faster your regeneration takes place.

 

Combined therapy is believed to:

  • Increases cellular growth
  • Increases Metabolic Activity
  • Reduces swelling around the nerve
  • Stimulates nerve function
  • Increases oxygen and blood directly to the nerve
  • Promotes wound healing
  • Anti-inflammatory action
  • Reduces scar tissue development

The patient has the ability to attain increased movement once again with an effective and favorable pain management treatment plan.

How are allergies and pain related?

What is the relationship between allergies and pain?

Allergies can create a generalized inflammatory state with systemic release of inflammatory cytokines, which may present as:

Muscle and joint pain, typically observed in food borne allergens such as gluten or gliaden.

Sinus congestion triggering migraine and cluster headaches, typically observed in aeroallergens such as pollens or molds

Aeroallergens such as dust, ragweed, pollen, and mold impact half of all Americans.   Symptomatic treatment with decongestants, histamine blockers, and steroids do not reduce the allergic potential of the allergen and do not change the course of disease. Many patients treated symptomatically become hyper sensitized and allergic to multiple additional antigens within three to five years, unless a desensitization immunotherapy protocol is initiated. Immunotherapy protocols use a low dose exposure to habituate the immune system to the allergen.

You might have allergies if you have any of the hollowing symptoms:

Sinus related issues (sinus pressure/pain, headaches, sinusitis) Restless sleep, challenges sleeping through the  night, snoring
Re-occurring Seasonal Colds Consistent or Re-occurring coughing
Chronic colds (lasting longer than 2 months) Feeling of fatigue, irritability, & restlessness
Migraine Headaches Asthma

Skin Conditions (dry and/or itchy skin, etc…)

 

Both allergies and pain are associated with overlapping inflammatory processes, with a resulting hypersensitivity of the central nervous system. Reciprocal signalling between immunocompetent cells in the central nervous system (CNS) is associated with pathological and chronic pain mechanisms. Glial cells, including parenchymal microglia, perivascular microglia, astrocytes and oligodendrocytes, constitute > 70% of the total cell population in the central nervous system. Glial cells have been identified as key neuromodulatory, neurotrophic and neuroimmune elements in the CNS. Neuronal excitability can be powerfully enhanced both by classical neurotransmitters derived from neurons, and by immune mediators released from CNS-resident microglia and astrocytes, and from infiltrating cells such as T cells. During autoimmune inflammation of the nervous system, microglia release and respond to several cytokines, including IL-1, IL-6, TNFα and IFNγ, which are instrumental in astrocytic activation, induction of cellular adhesion molecule expression and recruitment of T-leukocytes.

Left untreated, allergies can have a significant impact on an individual’s quality of life and wellbeing. Asthma is just one potential consequence of leaving allergies untreated.

Daily in the United States:

  • 30,000 People have an Asthma attack
  • 5,000 People visit the ER due to Asthma
  • 1,000 People are admitted to the Hospital, with an avg. hospital stay is 4.3 days
  • 11 people die from Asthma

36 states have laws prohibiting driving while under the influence of OTC and prescription antihistamines.

People are 50% more likely to have a work-related accident when using non-prescription sedating antihistamines.

A study in the American Journal of Managed Care reports that workers are 25% less productive for two weeks each year if they use sedating drugs to manage allergy symptoms.

 

 

What are aeroallergens?

Aeroallergens include pollen grains, biogenic waste, mold spores, and occupational allergens. Clinically significant aeroallergens are small proteins or glycoproteins, which are buoyant and able to travel long distances when propelled by wind such as pollen grains, biogenic waste, mold spores, and occupational allergens.

 

Pollen grains

Pollen grains are living male gametophytes (sperm) of plants and are microscopic in size. Ragweed is about 20µ in diameter; tree pollen is 20-60µ; and grass pollen is 30-40µ. High volumes of pollen are produced annually. A single ragweed plant can produce one million pollen grains in a single day. Some trees (conifers, for example) can release so much pollen that the microscopic grains form a cloud and can form a visible carpet on the ground. Ragweed pollen is so light that it can be transported hundreds of miles by the wind and has become one of the most significant sensitizing aeroallergens.

Biogenic waste

Dust mites are highly allergenic and cause significant symptoms of allergic rhinitis, sinus disease and bronchial asthma. Dust mites are tiny (.33 mm) barely visible, eight-legged insects. They eat human skin, animal dander, fungi and anything rich in protein. High humidity and warm temperatures allow dust mites to thrive and are found at their highest concentration in the temperate zones—particularly in people’s beds. They have an affinity for materials such as bedding, drapes, carpets and upholstery. In fact, dust mites are often most numerous right under your nose, as your head rests on your pillow.

German cockroaches are common in cities when apartments are heated. They produce potent allergens that are associated with asthma.

Dog and cat dander occur through desquamation of skin. Dander is skin flakes that contain highly allergenic, water-soluble proteins. Cat dander contains the potent Fel d 1 allergen, while dog dander contains the Can f 1 and Can f 2 allergens. Animal dander often remains in homes for many months, leading to persistent symptoms long after the pet’s removal. Further, dander can remain in air ducts or walls and hidden areas for years.

Mold Spores

Outdoor mold

Outdoor fungi are also called field fungi and thrive on plants decaying in the soil. Their spores are released in the highest numbers between the spring and fall, when humidity is high. Mold exposure is associated with a variety of allergy symptoms. One study indicated that children exposed to fungal spores had a 10% to 30% increase in asthma symptoms for every 1000 spores/m3 of air.

Indoor mold

Aspergillus and Penicillium are often referred to as “storage fungi” since they grow on dead and dying stored grains, rotting fruits and vegetables. These fungi on stored items in basements will appear as green mildew. Black-colored fungi is associated with Rhizopus and Stachybotrys.

Occupational allergens

Allergic reactions to aerosolized allergens in the workplace may result in occupational disability. Identification of occupational allergy early in its development may prevent permanent lung damage and long-term disability.

Although most allergy sufferers experience symptoms at home or outdoors, a smaller group of these individuals encounter potent allergens at work. Knowledge of potential workplace allergens can lead to early detection of occupational allergic disease. At first, symptoms might be mild, but they can progress to produce severe allergies—including permanent lung damage. These allergens are often unique to specific occupations and therefore, one must always consider the workplace as a source for aeroallergen exposure.

How do contact or food allergies effect pain?

For all intensive purposes, imagine the human body as a donut floating in space. The entire gastrointestinal system is a complex sensory monitoring system and a nutrient absorption system, it would be the center hole. The outer ring of the donut would be the skin. Food contact allergens presented to the surface of the donut interact with the surface of this donut, individuals with food allergies to substances such as gluten and gliaden develop a leaky gut by loosening the zonules (anchor point between cells) permitting other large molecules to transfer into the body and at the same time activate a large autoimmune neurological response, which often include pain mediators.

 

Allergy testing

Aero allergies are immediate hypersensitivity reactions caused by an IgE antibody, triggering the release of chemicals such as histamine. Because an IgE antibody causes such allergies, it is possible to perform allergy testing to determine the exact trigger and establish a specific diagnosis. One advantage is that skin-testing shares the same exact allergens used in immunotherapy, assuring that the treatment program incorporates all essential allergens.

 

Immunotherapy

Of all the therapies offered for respiratory allergy, injection therapy or immunotherapy is perhaps the most specific and effective treatment available in preventing recurrent symptoms in a hypersensitive patient. However, immunotherapy is only effective if the offending allergens are identified and incorporated into the allergy serum in adequate concentrations. Half-measures often prove inadequate in stubborn cases. A careful and comprehensive allergy history and skilled allergy testing are the basis for an effective treatment program.

 

Allergy injection treatment is carried out over a long period of time (3 – 6 years in most cases). At first, patients receive weak solutions of allergens. The dose is then gradually increased to induce tolerance without reactions. The goal is to achieve a high enough maintenance dose, which affords the best symptom relief. Improvement in symptoms usually lasts for years after completing a successful course of allergy injections.  85% of people treated with immunotherapy for hay fever may achieve symptom relief within the first year of starting immunotherapy.

Serious treatment options for serious foot pain

Nearly 60% of patient’s with chronic forefoot pain presenting to a podiatry practice have surgical intervention, yet only 50-60% of them get relief of foot pain long-term and 20% get significantly worse, requiring multiple surgeries. Accurate diagnosis is critical to appropriate treatment, common areas where foot pain is misdiagnosed include:

 

  • Plantar plate disruption

The metatarsophalangeal joint plantar plates are major stabilizers and form part of the plantar capsule. The plantar plates provide strength and support during ambulation. Disruption can lead to toe deformities.  The normal plantar plate is a slightly hyper echoic broad-curved band, which protects the metatarsal head and inserts onto the proximal phalanx. Plantar plate tears typically appear as hypo echoic defects.  The torn plantar plate is often swollen and hyper vascular in the acute phase of degeneration.

 

  • Adventitial Bursitis

Adventitial bursitis is acquired bursitis in the metatarsal fat pad as a result of trauma. Sonographically these areas may either be ill-defined or focal collections. These are generally compressible and hypo echoic, although complex collections may appear heterogeneous.

 

  • Synovitis

Joint effusions are compressible anechoic collections best seen on the dorsal aspect of metatarsophalangeal joints. Synovial proliferation appears on ultrasound as a thickening of the synovial layer. Hyper vascularity and bone erosions may also be present.

 

  • Morton’s Neuroma/ intermetatarsal bursitis

A Morton’s neuroma is caused by mechanical damage to the interdigital nerve, resulting in perineural fibrosis. On ultrasound it commonly appears as an ovoid hypo echoic mass, although the shape and echogenicity may vary. Intermetatarsal bursitis appears as a hypo echoic or anechoic zone in a normally echogenic webspace, generally dorsal to the interdigital nerve, although sometimes enveloping it. This soft tissue collection may become complex and heterogeneous with time. Dynamic assessment of a webspace will show poor compressibility of a neuroma and high compressibility of a bursitis (note: complex bursa may mimic a neuroma).  Treatment options include ultrasound guided cortisone or alcohol injection.

 

Morton’s neuroma or more appropriately entrapment syndrome

Common causes of forefoot pain include joint inflammation (arthritis, capsulitis & synovitis), plantar plate tears, tendinosis (“tendinitis”), bursitis and Morton’s neuroma.

A Morton’s neuroma occurs when scar tissue builds upon a nerve in between the toes known as the interdigital nerve (nerve between the digits, or toes). In Morton’s entrapment, the common plantar digital nerve, also referred to as the intermetatarsal nerve, gets compressed from forefoot plantar pressure in the late midstance and propulsive phases of gait against the distal margin of the transverse intermetatarsal ligament This is most frequently seen in women and is and is attributed to high heeled shoes. The pain is often severe and has an electric shock character to it.  Common symptom descriptions include some or all of the following: “It feels like my sock is wadded up under my foot,” “cramping,” “numbness,” “burning,” “radiating sensations into the adjacent toes,” “the inability to walk barefoot on a hard floor,” and “tingling.”   Others describe a feeling like having a pebble in their shoe or walking on razor blades.  Symptoms include: pain on weight bearing, frequently after only a short time. The nature of the pain varies widely among individuals. Some people experience shooting pain affecting the contiguous halves of two toes. Burning, numbness, and paresthesia may also be experienced.  Usually, patients with Morton’s entrapment demonstrate pain with plantar palpation of the interspace between the metatarsal heads.

As a true nerve entrapment no different in pathology from carpal tunnel syndrome, Morton’s entrapment treatment should be oriented toward decompression. Indeed, the treatment success rate of peripheral nerve decompression in Morton’s entrapment is higher than with surgical resection, has a much lower complication rate, and precludes serious complications associated with nerve excision.

Diagnostic lidocaine blocks are extremely beneficial in assisting in making an accurate diagnosis and can help the practitioner decide on a course of treatment, specifically when two adjacent interspaces are symptomatic.  It has generally been recommended that prior to surgical treatment for Morton’s entrapment, all methods of “conservative” care should be exhausted, including corticosteroid injections, application of offloading pads, sclerosing injections with alcohol or phenol, or radiofrequency ablation.

RADIOFREQUENCY

Radiofrequency nerve treatment is a technique, which has been used for over 10 years for the treatment of longstanding pain. Using local anesthesia, an electrode is placed into the tissue at the painful site and an electric current is delivered, generating heat that destroys the sensory nerve fiber.

The RF Procedure

A medical provider experienced in interventional procedures performs Radiofrequency ablation. The patient is placed in an appropriate position for the procedure; a diathermy pad is placed on the thigh and the injection site cleansed. Pain relief is achieved by injecting a local anesthetic around the nerve that is responsible for the patient’s pain. Once the nerve and area is anaesthetized (numbed), a fine needle is positioned in proximity to the nerve, with the position of which confirmed by imaging guidance (ultrasound or fluoroscopy).

A thin probe is then passed through the needle, which is connected to a generator that results in radiofrequency energy passing through the probe, resulting in heating of the probe tip. The result of this heat is to destroy the targeted nerve and therefore disrupting the ability of the nerve to transmit pain signals. Finally, long-term local anesthetic and cortisone are injected around the treated nerve in order to minimize discomfort, which may arise following the treatment. Treatment via RFA takes approximately 30 minutes. Further time spent at the clinic for post-procedure recovery may be suggested, depending on the exact nature of a patient’s condition. Ultrasound-guided RFA has successfully alleviated patients’ symptoms of Morton’s neuroma/ entrapment in >85% of cases. Less than 10% of patients progress to surgical intervention, such as endoscopic plantar fasciotomy.

ENDOSCOPIC PLANTAR FASCIOTOMY

EPF is an outpatient procedure. It takes about an hour to perform, and is be done at a hospital or a same-day surgical facility. Using special instrumentation we release the inside band of the plantar fascia responsible for causing your pain. After the procedure, you’ll be taken to a recovery area. As your foot heals, new tissue fills in the gap where the fascia was cut. This lengthens the fascia and reduces strain during foot movement. For best results, see your doctor as directed during the next few weeks or months. Physical therapy or stretching exercises are often prescribed to improve recovery. Wearing shoes with good support is essential for your long-term recovery.

 

 

 

 

Severe Head and Neck Pain

Caution:

If you’re having your worst migraine ever or symptoms that are unusual for you or frightening, see a doctor as soon as possible. You need to be sure this IS a Migraine and not something more serious such as a stroke. 

Caution:

Pregnant women should immediately alert their physician as many of the medications used to treat migraines can cause birth defects.

 

 

The goal of the Padda Institute Headache Section is to provide diagnosis and treatment that will help people who experience severe pain regain a better quality of life.  (The treatment needs of patients who have occasional mild headaches are significantly different from those patients whose attacks are frequent and completely disabling.)  If your quality of life is impacted from migraine, chronic head pain, or nerve pain in the face you need a plan of action from a team of highly experienced specialists. We provide a collaborative approach combined with the latest technology resulting in individualized care. Our goal is to provide effective, compassionate care to improve your quality of life.

Headaches are serious

Headache remains one of the most common health issues which challenge physicians and other health professionals, migraine is the 12th most disabling disorder in the United States..  The symptoms of head pain are a frequent cause of human suffering and disability.  According to a World Health Organization analysis, severe Migraine attacks are as disabling as quadriplegia (paralysis of both arms and legs).  Suicide attempts are three times more likely among people who have Migraine with aura than among people who do not have Migraine.  More than 1,400 American women with Migraine with aura die each year from cardiovascular diseases compared to women who do not have Migraine.

Migraines permanently affect your brain

Some 37 million Americans suffer from migraines, those incredibly painful and often debilitating headaches. While they’ve been known to knock a person out, migraines weren’t thought to permanently affect the brain – until now.  A study published in the journal Neurology suggests migraines permanently alter brain structure in multiple ways.  The risk of white matter brain lesions increased 68% for those suffering migraines with aura, compared to non-migraine sufferers. Those who suffered from migraines without aura saw that increased risk cut in half (34%), but they too could get lesions in the part of the brain that is comprised of nerve fibers.  Migraine affects about 10 to 15% of the general population and can cause a substantial personal, occupational and social burden.  According to the American Migraine Foundation, migraines cost the United States more than $20 billion a year in both direct medical expenses like doctor visits and medication and indirectly when employees miss work resulting in lost productivity.

For many patients with headache, an organized, multidisciplinary headache center environment is necessary to provide the entire spectrum of headache management.

 

  • Patients in whom comprehensive services are essential to address the multifunctional components of their headaches.
  • Patients who have not responded to medication and have a history of recurring acute care needs or progressive persistent headache.
  • Patients who have undergone multiple diagnosis and therapeutic interventions yet the diagnosis remains uncertain or questionable.
  • Patients who have had frequent emergency room visits, who have used hospital inpatient services excessively, and who have overused different oral analgesics, including opiates, or who have been treated repeatedly with intramuscular or intravenous medications.

 

 

The History of Headaches

The clinical entity of headache dates back to ancient times.  As early as the dawn of civilization, primitive headache remedies included procedures aimed at ridding the body of the “demons and evil spirits” that were believed to cause headaches.  As early as the Neolithic period dating back to 7000 BC, skulls have been found bearing man made holes (called trephination) presumably done for medical reasons which may have included the treatment of headache.  Skulls demonstrating trepanation have also been found in Peru dating back to the thirteenth century.  The writings of the early Greeks referred to headache as a serious medical condition.

Hippocrates (400 BC) may have been the first to describe the clinical symptoms of migraine.  In the historical Hippocratic books Hippocrates discussed what appears to have been the visual aura that can precede migraine.  The term “migraine’ itself is derived from the Greek word hemicrania. Throughout history, there have been famous individuals such as Plato, Thomas Willis, Erasmus Darwin (Charles Darwin’s grandfather), and others who have contributed to our understanding of headache. More recent scholars, such as Dr Harold Wolff, played an important role in our classification of different types of headache and their treatment. Following his classic 1948 publication of the first edition of Wolff’s Headache, it was Dr Wolff who introduced important scientific concepts which have served to modernize the study of headache.  Since that publication there has been an explosion in headache research which has resulted in our better understanding of this clinical condition.

There are now scientific mechanisms which more clearly define the pathophysiology of some headaches such as migraine.  This has also led to the development of new migraine specific medications, specialized pain management techniques, and ultimately more effective treatment opportunities.

Migraines have affected people for centuries and played an influential role throughout world history. Many famous and accomplished people have experienced severe headaches.  Julius Caesar, Napoleon, Ulysses S. Grant and Robert E. Lee; great painters Vincent Van Gogh, Georges Seurat and Claude Monet,; and famous authors Virginia Woolfe, Cervantes and Lewis Carroll all experienced migraines. Thomas Jefferson wrote the Declaration of Independence during an intense period of productivity after being bedridden for six weeks with a migraine.  The famous authors Virginia Woolf, Cervantes (best known for Don Quixote) and Lewis Carroll (Alice’ Adventures in Wonderland) had migraine. There is even evidence to suggest that at least some of Alice’s Adventures were based on Carroll’s personal migraine visual aura perceptions. As Cheshire Cat observed, “One pill makes you smaller; one pill makes you larger, the pills mother gives you do nothing at all”.  There has been literature which indicates that Thomas Jefferson’s headaches were so severe and debilitating that they often interfered with his ability to function.  As he wrote to Martha Jefferson in February 18, 1784, “Having to my habitual ill health….lately added an attack of my periodical headache; I am obliged to avoid reading, writing, and almost thinking”.  In March 1807, while still President, Jefferson wrote “…Indeed, I have but little moment in the morning in which I can either read, write, or think, being obliged to be shut up in a dark room from early in the forenoon till night, with a periodical headache”.

Headache sufferers constitute one of the largest groups of patients within a neurological practice.  More patients who visit doctors complain of headache than any other single ailment. Headache and migraine in particular, may be considered as a universal human condition which continues to be under diagnosed, misdiagnosed and/or mistreated.  Whereas in some individuals, headache may be an occasional episodic, sometimes nuisance, for others the symptoms of headache may be a manifestation of a disabling chronic disease.  In the latter group, headache disrupts daily routines and impairs quality of life.  The frequency, severity, and even life consequences of headache sufferers vary widely.  The causes of headache are different in different individuals.

 

Range of Disorders:

Each year, millions of Americans suffer from chronic headaches.  There are four main headache types: tension, cervicogenic, migraine and cluster.

  • Tension headaches are the most common and may be described as a mild to moderate constant band-like pain, tightness, or pressure around the forehead or back of the head and neck.

 

  • While cervicogenic headaches are slightly less common and are caused by any number of conditions in the neck, causing referred pain, most often the cervical facets or the cervical discs.  Some studies suggest that the trigeminal sympathetics and parasympathetics mediate pain from the region of the Occipital Nerve, such to the degree that the Occipital Nerve may be considered the “V4” of the trigeminal.  Cervicogenic pain can trigger Migraine headaches and Cluster headaches.

 

  • Migraine headaches are severe headaches that are described as a chronic, throbbing head pain that can cause significant pain for hours or even days.  Symptoms can be so severe that light or sound can cause exacerbation and most patients must find a dark quiet room to lie down.  The typical Aura of Migraines is only present in 25-30% of all cases.

Status Migrainosus: A rare, sustained and severe type of migraine headache, lasting more than 72 hours that is characterized by intense pain and nausea, often leading to hospitalization.

Chronic daily headaches occur frequently, usually more than 15 days per month. Chronic daily headaches are classified as either long duration (lasting more than four hours) and short duration (lasting less than four hours). The majority of people who experience chronic daily headaches have long-duration headaches.

Medication overuse headaches, sometimes called rebound headaches, occur when people who experience migraine or tension headaches take too much analgesic or anti-migraine medication. When the effect of one dose wears off, the next headache occurs and another round of medication is taken. A vicious cycle is created of ever-increasing headaches and more frequent medication use.  Taking Migraine abortive medications, pain relievers, or alternating them more than two or three days a week can cause medication overuse headache.

Menstrual migraine is a headache that occurs during the menstrual cycle. It can occur two days before and up to three days after the beginning of a woman’s period. Although the cause is not explicitly known, menstrual migraine may be triggered by changes in hormone levels. The most likely cause is the fall in estrogen levels that takes place just before the beginning of menses.  When women experience menopause naturally, 1/3 experience worse Migraines. When women experience menopause following a hysterectomy, 2/3 experience worse Migraines.

Studies have shown that 90% of what people think are sinus headaches are really Migraines. A sinus headache is very rare without an infection.

  • Cluster headaches, also known as suicide headaches, are excruciating unilateral headaches of extreme intensity. The duration of the common attack ranges from as short as 15 minutes to three hours or more. The onset of an attack is rapid, and most often without the preliminary signs that are characteristic of a migraine. They are marked by repeated, short-lasting attacks of excruciating, unilateral head pain of short duration.  A cluster headache may be accompanied by redness or tearing of the eye and nasal congestion or runny nose. Often mistaken for sinus or migraine headaches, cluster headaches are characterized by sharp, stabbing pain in or around the eye, temple, forehead or cheeks.
  • Atypical facial pain of all types including trigeminal neuralgia

To assure an accurate diagnosis, we collect an extensive medical history and conduct a comprehensive neurological exam. At times we request a specialized MRI of the brain and neck or blood tests that search for causes of headache including hormone levels, vitamin levels, or markers of an overactive immune system. After the evaluation, treatment options are discussed including medications, lifestyle modification, pain relieving procedures and alternative therapies.  Nearly 30% of patients with dental pain after dental procedures are actually a form of trigeminal neuralgia.

 

Outpatient Treatment

For many people, medication is required to control their headaches. Avoiding the triggers which initiate headache onset is the most important step. There are two categories of headache medication: abortive and prophylactic.

 

  • Trigger Management

Trigger management is key to preventing a migraine attack, migraines don’t just happen; they have triggers.  Trigger factors are those circumstances or influences that can cause a migraine. Trigger factors vary from person to person; if recognized and avoided, a person may prevent a migraine from developing.

Examples of triggers include changes in weather or air-pressure, bright sunlight or glare, fluorescent lights, chemical fumes, menstrual cycles, and certain foods and food products, such as processed meats, red wine, beer, dried fish, fermented cheeses, aspartame and MSG.

  • Preventive or Prophylactic Medication Therapy

Prophylactic drugs are taken daily to prevent headaches. They may be prescribed for people who experience frequent severe headaches, usually two or more per month. These drugs may be taken until a person’s headaches are under control. Generally, the lowest effective dose is used for the shortest period possible. Examples of prophylactic drugs are anti-depressants, beta blocker and calcium-channel blockers.

Many people who take preventive or prophylactic medications will also need to take attack-aborting medications to relieve pain and other symptoms.

  • Abortive Medication Therapy

Attack-aborting medications can relieve the severity and/or the duration of migraine headaches and their related symptoms. In general, most attack-aborting medication should be taken as early as possible in an attack.

Many people who experience migraines or other severe headaches can recognize their early symptoms, allowing them to intervene early with the attack-aborting medication. This may allow them to avoid a more severe, prolonged episode. Attack-aborting medications include cerebral vascoconstrictor abortive agents and non-vasoconstrictive abortive agents.

Specialized Treatment Options for Headache, Migraine and Facial Pain

Our team cares for many patients each year which empowers countless people to achieve substantial improvement. Some of our specialized treatments offered include peripheral nerve injections, which numb the nerves of the scalp to shut off chronic migraine. On average, the injections can give patients weeks to months of benefit. In rare cases, our team provides occipital nerve stimulation by a surgically implanted device that delivers an electric charge to nerves in the back of the scalp to treat migraine, cluster headache, and other types of facial pain that doesn’t respond well to other treatments. This is a treatment few other centers offer.

We also offer a number of alternative therapies with special focus on nutraceuticals – nutritional supplements – and vitamin therapies that have anti-pain or anti-migraine suppressing properties. Also available is pain psychology which uses relaxation strategies and biofeedback to reduce migraine. Our clinic embraces a specialized hormone therapy, called bioidentical hormone replacement therapy. This is where a patient’s hormonal status is monitored and individualized hormonal therapy is provided to normalize the body’s natural cycle and reduce migraine or head pain associated with hormonal dysfunction. We also offer acupuncture.

 

Advanced therapies

  • Spenopalatine Block

The Sphenopalatine Gangion Nerve Block (SPG Nerve Block) is both a  preventative and abortive technique, and may infact prevent trigger activation altogether.

The Sphenopalatine ganglion (SPG) nerve block and the Trigeminal Nerve Block is a fast, highly effective, non-invasive treatment option for migraines and headaches without the use of pills or injections. This treatment uses a unique transnasal catheter to eliminate the pain in a safe and painless way. Aside from migraine and headache, It has been providing successful relief to a variety of painful conditions including trigeminal neuralgia.

Technical:

The sphenopalatine ganglion (pterygopalatine, nasal, or Meckel’s ganglion) is located in the pterygopalatine fossa, posterior to the middle nasal turbinate. It is covered by a 1- to 1.5-mm layer of connective tissue and mucous membrane. This 5-mm triangular structure sends major branches to the gasserian ganglion, trigeminal nerves, carotid plexus, facial nerve, and the superior cervical ganglion. The sphenopalatine ganglion can be blocked by topical application of local anesthetic or by injection.

  • Trigeminal Blockade

Trigeminal neuralgia is an extremely painful condition that affects the trigeminal nerve in the face, which is also called the fifth cranial nerve.  The Trigeminal Nerve is often called the Dentist’s Nerve because it goes to the teeth, jaw muscles, jaw joints (TMJ),and periodontal ligament. Trigeminal innervation of the sinuses, eustacian tubes, tensor of the ear drum (tensor tympani), soft palate, tongue and meninges of the brain explain why there are so many disorders associated with jaw function, TMJ and TMD. The trigeminal nerve plays a very important role in the face, being responsible for sensing touch, pressure, pain and temperature in the jaw, gums, forehead and around the sensitive eye area. Since it controls sensation in almost the entire face, pain in the trigeminal nerve can affect many different parts of the face.  Many people speculate that most atypical facial pain, most dental pain, most sinus induced headache, and most headache originating from the base of the skull results from trigeminal activation.

 

About Vitamin D

What is Vitamin D?

Vitamin D is not truly a vitamin.

Compounds are called vitamins only if they cannot be synthesized , and must be obtained from the diet.  Vitamin D, however, is produced in sufficient quantity in the presence of sunlight and cholesterol and should not be considered a vitamin.

In addition, cholesterol is the precursor for most hormones, and Vitamin D should really be viewed as a light dependent fat-soluble hormone.

Historically we have thought that Vitamin D was involved in the absorption of Calcium and Phosphorous from the intestine, and were concerned primarily about its involvement as an osteoporosis risk factor.  However, the reality is that Vitamin D is involved in a variety of metabolism functions, not just bone health.

 

  • Abnormal low levels of Vitamin D are associated with increased risk of death and disability from cardiovascular disease and cancer.

 

  • Vitamin D is also involved in general metabolism and reducing obesity through effects on testosterone, thyroid hormones, and insulin.

 

  • Vitamin D is also involved in neurologic autoimmune dysfunctions such as Multiple Sclerosis and Alzheimer’s.

 

Why is my Vitamin D level low?

There are a variety of  reasons why Vitamin D levels are found to be low in an otherwise healthy person:

Inadequate Vitamin D intake, which could be a function of poor diet or a diet contaminated with other fat-soluble agents, such as organochlorine pesticides, which prevent adequate absorption.

Inadequate sunlight exposure, due in part to industrialization and conversion to an indoor lifestyle and also to medical recommendation to reduce sunlight exposure and in fact even use sunlight blocking agents.  Sunscreen blocks sunlight and an SPF (sun protection factor) of 8 blocks 95% of the sun, so there needs to be a careful balance between over- and under- sun exposure.

Drinking milk is not a good source of Vitamin D, as an 8 oz glass of fortified milk contains merely 100 IU in comparison to 15 minutes of sun exposure which generates 20,000 IU of Vitamin D.

 

How do I replace my Vitamin D?

We typically replace Vitamin D only if the measured levels are found to be low; and this is usually associated with other endocrine abnormalities which can be addressed simultaneously.  Vitamin D replacement therapy is done by oral supplement, typically using a once a week preparation.  Retesting of the level should be done after three to six months of consistent replacement.  Replacing Vitamin D should only be done after a blood test confirms that the levels are low, because too much Vitamin D can also cause serious complications.

 

Where to buy Vitamin D?

Vitamin D3 is typically prescribed, but is also available over the counter.  I typically recommend purchasing it inexpensively through Amazon, since a two year supply of Vitamin D3 (50,000 units) taken once a week is cheaper than copay for a one month supply from the traditional pharmacy.

 

Electrodiagnostics EMG NCS (dermatomes and myotomes)

 

Electrodiagnostics (EDX) testing is used to evaluate the integrity and function of the peripheral nervous system (most cranial nerves, spinal roots, plexi, and nerves), NMJ, muscles, and the central nervous system (brain and spinal cord). EDX testing is performed as part of an EDX consultation for diagnosis or as follow-up of an existing condition. EDX studies can provide information to:

 

 

 

 

  • Identify normal and abnormal nerve, muscle, motor or sensory neuron, and NMJ functioning.
  • Localize region(s) of abnormal function.
  • Define the type of abnormal function.
  • Determine the distribution of abnormalities.
  • Determine the severity of abnormalities.
  • Estimate the date of a specific nerve injury.
  • Estimate the duration of the disease.
  • Determine the progression of abnormalities or of recovery from abnormal function.
  • Aid in diagnosis and prognosis of disease.
  • Aid in selecting treatment options.
  • Assists in following response to treatment by providing objective evidence of change in neuromuscular function.
  • Localize correct locations for injection of intramuscular agents (e.g., botulinum toxin).

 

Electromyography (EMG) is a technique for evaluating and recording the electrical activity produced by skeletal muscles.  An EMG detects the electrical potential generated by muscle cells when electrically or neurologically activated.  Often, EMG testing is performed with another test that measures the conducting function of nerves, called a nerve conduction study (NCS). These electrodiagnostics tests (EMG and NCS) are often performed at the same office visit and by the same personnel, the risks and procedures generally apply to both tests.

 

In some medical conditions the electrical activity of the muscles or nerves is not normal. Finding and describing these electrical properties in the muscle or nerve may help diagnose your condition.  EDX may aid with the diagnosis of nerve compression or injury (such as carpal tunnel syndrome), nerve root injury (such as sciatica), and with other problems of the muscles or nerves. Less common medical conditions include amyotrophic lateral sclerosis, myasthenia gravis, and muscular dystrophy.  EMG is most often used when people have symptoms of weakness, and examination shows impaired muscle strength. It can help to tell the difference between muscle weakness caused by injury of a nerve attached to a muscle and weakness due to neurologic disorders.

Dorsal (back) of spinal cord transmits sensory information from sensory units to brain, Ventral (front) of cord transmits motor information from brain to muscle
Needle electrode stimulation allows evaluation of nerve to muscle function

 

Electrical impulses are recorded for detailed analysis after the EMG test is completed.

 

 

Risks

People usually have a small amount of discomfort during EMG testing because of pin insertion. Disposable needles are used so there is no risk of infection.

 

During nerve conduction studies, small electrodes are taped to the skin or placed around fingers. You typically experience a brief and mild shock, which may be a bit unpleasant. Most people find it only slightly annoying.

 

It is very important to note that most EMG/NCV tests are not 100% accurate. Most physicians will admit that the tests have at least a 10% margin of error. Very often individuals with nerve damage will have normal EMG/NCV tests even though they are experiencing nerve damage.

 

During the Procedure

During EMG, small pins or needles are inserted into muscles to measure electrical activity. The needles are different than needles used for injection of medications. They are small and solid, not hollow like hypodermic needles. Because no medication is injected, discomfort is much less than with shots.

 

You will be asked to contract your muscles by moving a small amount during the testing.

 

With nerve conduction studies, small electrodes will be taped to your skin or placed around your fingers. You typically will experience a mild and brief tingling or shock, which may be a bit unpleasant.

 

The person who administers the test will explain the procedure. Often muscle activity is monitored through a speaker during the test, which may make a popping or soft roaring noise. The EMG technician will be looking at an oscilloscope, which looks like a small TV set during the procedure.

 

How long does EDX take?

Testing may take 30-60 minutes. The nerve conduction part of the test usually takes longer than the needle exam because one needs to make calculations and measurements during it. On average, if one extremity is studied, the nerve conductions take anywhere between 15 and 30 minutes. The needle exam for one extremity usually takes 15 to 20 minutes. You can count on being in the examination room for about one hour if only one extremity is requested; longer if more extremities need to be tested.

Carpal Tunnel Syndrome

For suspected carpal tunnel syndrome (CTS), bilateral median motor and sensory NCSs are often indicated. The studies in the contralateral asymptomatic limb serve as controls in cases where values are borderline and may establish the presence of bilateral CTS, which is a frequent finding. Two to 4 additional sensory or mixed NCSs can be compared to the median sensory NCSs to increase the diagnostic sensitivity of the testing. The additional sensory NCSs and an additional motor NCS (usually ulnar) are indicated to exclude a generalized neuropathy or multiple mononeuropathies. If 2 sensitive sensory NCSs are performed to start, additional sensory testing on the same limb is rarely needed. For suspected bilateral CTS, bilateral median motor and sensory NCSs are indicated. Up to 2 additional motor and 2 additional sensory NCSs are often indicated. The extent of the needle EMG examination depends on the results of the NCSs and the differential diagnosis considered in the individual patient.

Delayed conduction due to entrapment syndromes such as carpal tunnel and tarsal tunnel are best evaluated with NCS. If atrophy of muscles occurs it will also be evident as denervation by EMG.

Additional testing may be indicated in patients with a differential diagnosis which includes peripheral neuropathy, cervical radiculopathy, brachial plexopathy, or more proximal median neuropathy.

 

Radiculopathy

A minimal evaluation for radiculopathy includes 1 motor and 1 sensory NCS and a needle EMG examination of the involved limb. However, the EDX testing can include up to 3 motor NCSs (in cases of an abnormal motor NCS, the same nerve in the contralateral limb and another motor nerve in the ipsilateral limb can be studied) and 2 sensory NCSs. Bilateral studies are often necessary to exclude a central disc herniation with bilateral radiculopathies or spinal stenosis or to differentiate between radiculopathy and plexopathy, polyneuropathy, or mononeuropathy. H reflexes and F waves can provide useful complementary information that is helpful in the evaluation of suspected radiculopathy and can add to the certainty of electrodiagnostic information supporting a diagnosis of root dysfunction.

 

 

Mononeuropathy and Polyneuropathy/ Mononeuropathy Multiplex

Mononeuropathy and polyneuropathy/mononeuropathy multiplex are entirely different conditions and must be considered separately. Mononeuropathy comprises focal lesions of a single peripheral nerve. Polyneuropathy comprises diseases in which there is a bilaterally symmetric disturbance of peripheral nerve functions. Mononeuropathy multiplex comprises multifocal isolated lesions of more than 1 peripheral nerve.

 

Mononeuropathy

To determine the level of the lesion in a focal mononeuropathy, and in order to exclude radiculopathy, plexopathy, or polyneuropathy, it may be necessary to study 3 motor and 3 sensory nerves including the clinically affected nerve, the same nerve on the contralateral side, and an unaffected ipsilateral nerve. F-wave studies provide additional diagnostic information. A needle EMG examination in the affected limb is indicated.

 

Polyneuropathy/MononeuropathyMultiplex

In order to characterize the nature of the polyneuropathy (axonal or demyelinating, diffuse or multifocal) and in order to exclude polyradiculopathy, plexopathy, neuronopathy, or multiple mononeuropathies, it may be necessary to study 4 motor and 4 sensory nerves, consisting of 2 motor and 2 sensory NCSs in 1 leg, 1 motor and 1 sensory NCS in the opposite leg, and 1 motor and 1 sensory NCS in 1 arm. H-reflex studies and F-wave studies from 2 nerves may provide additional diagnostic information. At least 2 limbs should be studied by a needle EMG examination. Studies of related paraspinal muscles are indicated to exclude some conditions such as polyradiculopathy.

 

Myopathy

To diagnose a myopathy, a needle EMG examination of 2 limbs is indicated. To help exclude other disorders such as polyneuropathy or neuronopathy, 2 motor and 2 sensory NCSs are indicated. Two repetitive motor nerve stimulation studies may be performed to exclude a disorder of neuromuscular transmission.

 

Motor Neuronopathy

In order to establish the diagnosis of motor neuronopathy (for example, amyotrophic lateral sclerosis [ALS or Lou Gehrig’s disease]) and to exclude other disorders in the differential diagnosis, such as multifocal motor neuropathy or polyneuropathy, up to 4 motor nerves and 2 sensory nerves may be studied. Needle EMG of up to 4 extremities (or 3 limbs and facial or tongue muscles) is often necessary to document widespread denervation and to exclude a myopathy. One repetitive motor nerve stimulation study may be indicated to exclude a disorder affecting neuromuscular transmission.

 

Plexopathy

To characterize a brachial plexopathy and to differentiate it from cervical radiculopathy and mononeuropathies, it is often necessary to study all major sensory and motor nerves that can be easily studied in both upper extremities (radial, median, ulnar, and medial and lateral antebrachial cutaneous sensory; radial, median, ulnar, and possibly axillary and musculocutaneous motor) and to perform a needle EMG examination in both upper extremities. To characterize the lumbosacral plexopathy and to differentiate it from lumbar radiculopathy and mononeuropathies, it is often necessary to study all major sensory and motor nerves that can be easily studied in both lower extremities (superficial peroneal and sural sensory; peroneal and posterior tibial motor) and to perform a needle EMG examination in both lower extremities. F-wave studies in the motor nerves and soleus H reflexes also provide useful information.

 

Neuromuscular Junction

To demonstrate and characterize abnormal neuromuscular transmission, repetitive nerve stimulation studies should be performed in up to 2 nerves and SFEMG in up to 2 muscles. If any of these are abnormal, up to 2 motor and 2 sensory NCSs may be performed to exclude neuropathies that can be associated with abnormal neuromuscular transmission. At least 1 motor and 1 sensory NCS should be performed in a clinically involved limb, preferably in the distribution of a nerve studied with repetitive stimulation or SFEMG. At least 1 distal and 1 proximal muscle should be studied by a needle EMG examination to exclude a neuropathy or myopathy that can be associated with abnormal repetitive stimulation studies or SFEMG. At least 1 of the muscles should be clinically involved and both muscles should be in clinically involved limbs.

 

Timing of Testing After an Injury

In combination, NCSs and a needle EMG examination may be most helpful when performed several weeks after the injury has occurred. However, NCSs are often useful acutely after nerve injury, for example, if there is concern that a nerve has been severed. In fact, if studies are delayed, the opportunity to precisely identify the region of injury or to intervene may be lost. In some cases, even needle EMG testing performed immediately after a nerve injury may demonstrate abnormal motor unit action potential (MUAP) recruitment and/or provide baseline information that can be helpful to document preexisting conditions, date the injury, or serve as a baseline for comparison with later studies.

 

Because of the variability of different nerve injuries, a standard rule on the timing of EDX testing cannot easily be established and the AAEM does not have specific recommendations in this regard. In all instances, the AAEM encourages dialogue between physicians and payors and encourages the appropriate use of the physician’s clinical judgment in determining when studies are most appropriately performed and what studies should be conducted.

 

Frequency of Electrodiagnostic Testing in a Given Patient

There are many clinical situations where good medical management requires repeat testing, such as in the following examples:

 

  • Second diagnosis. Where a single diagnosis is made on the first visit, but the patient subsequently develops a new set of symptoms, further evaluation is required for a second diagnosis.
  • Inconclusive diagnosis. When a serious diagnosis (e.g., ALS) is suspected but the results of the needle EMG/NCS examination are insufficient to be conclusive, 1, or even more, follow-up studies are needed to establish or exclude the diagnosis.
  • Rapidly evolving disease. Initial EDX testing in some diseases may not show any abnormality (e.g., Guillain-Barré syndrome) in the first 1 to 2 weeks. An early diagnosis confirmed by repeat electrodiagnosis must be made quickly so that treatment can begin. Follow-up testing can be extremely useful in establishing prognosis and monitoring patient status.
  • Course of the disease. Certain treatable diseases such as polymyositis and myasthenia gravis follow a fluctuating course with variable response to treatment. The physician treating such patients needs to monitor the disease progress and the response to therapeutic interventions. The results of follow-up evaluations may be necessary to guide treatment decisions.
  • Unexpected course or change in course of the disease. In certain situations, management of a diagnosed condition may not yield expected results or new, questionably related problems may occur (e.g., failure to improve following surgery for radiculopathy). In these instances, reexamination is appropriate.
  • Recovery from injury. Repeat evaluations may be needed to monitor recovery, to help establish prognosis, and/or to determine the need for and timing of surgical intervention (e.g., traumatic nerve injury).

 

 

Repeat EDX consultation is therefore sometimes necessary and, when justifiable, should be reimbursed. Reasonable limits can be set concerning the frequency of repeat EDX testing per year in a given patient by a given EDX consultant for a given diagnosis. The following numbers of tests per 12-month period per diagnosis per physician are acceptable:

 

  • Two tests for carpal tunnel-unilateral, carpal tunnel-bilateral, radiculopathy, mononeuropathy, polyneuropathy, myopathy, and NMJ disorders.
  • Three tests for motor neuronopathy and plexopathy.

 

 

 

Spinal nerves have motor fibers and sensory fibers. The motor fibers innervate certain muscles, while the sensory fibers innervate certain areas of skin. A skin area innervated by the sensory fibers of a single nerve root is known as a dermatome. A group of muscles primarily innervated by the motor fibers of a single nerve root is known as a myotome. Although slight variations do exist, dermatome and myotome patterns of distribution are relatively consistent from person to person.

 

The ventral (anterior) gray matter of the spinal cord contains nerve cells that send axon fibers out, through the nerves, to their end points on the muscles that they activate. Sensory information from the body and arriving instructions from the brain all cause movement by giving instructions to these “motor neurons” in the spinal cord gray matter.

 

Spinal Cord Segmental Myotomes and Dermatomes

Sensory dermatomes in blue, motor myotomes in yeallow

 

 

Myotomes – Relationship between the spinal nerve & muscle and are best evaluated with EMG

Dermatomes – Relationship between the spinal nerve & skin and a combination of EMG and NCS is used to define pathology.

 

Myotomes

Each muscle in the body is supplied by a particular level or segment of the spinal cord and by its corresponding spinal nerve. The muscle, and its nerve make up a myotome. This is approximately the same for every person and are as follows:

Myotome muscle EMG

 

  • C3,4 and 5 supply the diaphragm (the large muscle between the chest and the belly that we use to breath).

 

  • C5 also supplies the shoulder muscles and the muscle that we use to bend our elbow

 

  • C6 is for bending the wrist back.

 

  • C7 is for straightening the elbow.

 

  • C8 bends the fingers.

 

  • T1 spreads the fingers.

 

  • T1 –T12 supplies the chest wall & abdominal muscles.

 

  • L2 bends the hip.

 

  • L3 straightens the knee.

 

  • L4 pulls the foot up.

 

  • L5 wiggles the toes.

 

  • S1 pulls the foot down.

 

  • S3,4 and 5 supply the bladder. bowel and sex organs and the anal and other pelvic muscles.

 

Spinal Cord Segmental Dermatomes

Dermatome is a Greek word which literally means “skin cutting”. A dermatome is an area of the skin supplied by nerve fibers originating from a single dorsal nerve root.  The dermatomes are named according to the spinal nerve which supplies them. The dermatomes form into bands around the trunk but in the limbs their organisation is more complex as a result of the dermatomes being “pulled out” as the limb buds form and develop into the limbs during embryological development.

 

In diagrams or maps, the boundaries of dermatomes are usually sharply defined. However, in life there is considerable overlap of innervation between adjacent dermatomes. Thus, if there is a loss of afferent nerve function by one spinal nerve sensation from the region of skin which it supplies is not usually completely lost as overlap from adjacent spinal nerves occurs: however, there will be a reduction in sensitivity.

Different parts of the spinal cord provide innervation to the body, organized as dermatomes.
Lumbar radiculopathy, commonly referred to as sciatica.
Neck injury can cause pain in the hands and arms, referred to as cervical radiculopathy.