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ADL Austin Torch of Liberty Dinner

Capitol Pain Institute is proud to be an official sponsor of this Thursday’s Anti-Defamation League Event at the Four Seasons in Austin, Texas. “We’re very excited about this and we consider it an honor to be a sponsor for this great event,” said Dr. Matthew Schocket, founder of Capitol Pain Institute.

ADL Austin Torch of Liberty Dinner

Start:
September 18, 2014 6:00 pm
End:
September 18, 2014 10:00 pm
PinExt ADL Austin Torch of Liberty Dinneremail ADL Austin Torch of Liberty Dinner

Join more than 600 community leaders and members at the Four Seasons to honor Susan and Bobby Epstein and Marcia Levy and to celebrate ADL Austin’s many successes in its fight to end discrimination and ensure fair treatment and equality for all.

TORCH OF LIBERTY AWARD DINNER

TORCH OF LIBERTY HONOREES
SUSAN & BOBBY EPSTEIN

AUDREY AND RAYMOND MAISLIN HUMANITARIAN HONOREE
MARCIA LEVY

EVENT CO-CHAIRS
JENNIFER GREENBLUM & JOHNNA JONES
JEFF NEWBERG, ANDY PASTOR, & KIRK RUDY

KEYNOTE SPEAKER
SHARON ROBINSON
Author and Educational Consultant, Major League Baseball

THURSDAY
SEPTEMBER 18, 2014
FOUR SEASONS | AUSTIN, TEXAS

Learn more and register now at http://bit.ly/Yvygqs

Treatment of Painful Diabetic Neuropathy

Finding an effective treatment of painful diabetic neuropathy can be extremely frustrating, both for the individual in pain and for their loved ones desperately trying to find a solution.

Diabetic neuropathy is a nerve disorder caused by high blood glucose and other complications associated with having diabetes for a long time. The resulting nerve damage can be felt as numbness or pain in feet, lower legs, hands or arms. If you have painful diabetic neuropathy (PDN), you may experience that pain as tingling, burning, stabbing, deep aching or greater at the touch—especially at night. Sometimes the pain can come on fast and be severe.

According to the National Institute of Diabetes, most people with diabetes develop some form of neuropathy. It is more common if you have had diabetes for more than 25 years and have problems controlling your blood sugar, have high levels of blood fat and blood pressure, or are overweight.

Treatment

Doctors diagnose diabetic neuropathy based on symptoms and a physical exam. They may check your blood pressure, heart rate, muscle strength, reflexes and sensitivity to position changes, vibration, temperature or light touch. Once diagnosed, treatment can involve:

  1. Control of blood glucose levels

First, blood glucose levels must be brought within the normal range to help prevent further nerve damage. According to a Diabetes Control and Complications Trial, tight control of glucose levels can reduce the incidence of neuropathy by 60%.

  1. Prescribed oral medications

Diabetic Neuropathy 300x225 Treatment of Painful Diabetic NeuropathyBefore you reach for the usual painkillers, it might be worth getting a diagnosis from your doctor. Over-the-counter pain medicines are not recommended: they may not work well for treating nerve pain and can have serious side effects.

You do not have to be depressed for an antidepressant to help relieve your nerve pain; antidepressants are the most common form of treatment. According to the National Institute of Diabetes, drug options include tricyclic antidepressants (e.g. Norpramin, Pertofrane), other antidepressants such as duloxetine (Cymbalta), anticonvulsants such as pregabalin (Lyrica), and various opiods and opioid like drugs. Duloxetine and pregabalin are approved by the U.S. Food and Drug Administration specifically for treating PDN.

  1. Topical medications

Some people experience pain relief with treatments applied to the skin. According to the National Institute of Diabetes, these can include nitrate sprays, capsaicin cream and lidocaine patches (Lidoderm, Lidopain) for the feet, alpha-lipoic acid (an antioxidant) or evening primrose oil.

  1. Therapies and more

Others find that acupuncture, biofeedback or physical therapy help relieve their pain. Less studied options may include electrical nerve stimulation, magnetic therapy and laser or light therapy. However, new clinical trials of therapies happen all the time. Also, if your feet and legs are very sensitive to the touch, then a device called a bed cradle can help keep sheets and blankets away from the skin.

Treatment of painful diabetic neuropathy is complex and may involve a combination of medications or treatments. Patient suitability, benefits and potentially adverse side effects need to be considered for any treatment, but there is hope.

Get help by contacting us at the Capitol Pain Institute in Texas. Doctors here are pain management specialists, equipped to diagnose your specific condition and to find the most effective pain relief treatment to help relieve your pain. Instead of sitting there in pain, start to reclaim your life by booking an appointment now!

The Two Faces of Pain: Acute and Chronic

Living with pain has a debilitating impact on people. Whether this pain is associated with a previous injury or a result of a disease, it is important to understand where it comes from, how to address it, and how to explain it to those closest to you. Let us explore the two faces of pain: acute and chronic.

Acute pain

Acute pain is pain that lasts less than 3 to 6 months, or pain directly related to an injury or tissue damage. This type of pain consists of acute chronic pain texas 300x171 The Two Faces of Pain: Acute and Chronicthat which is associated with small burns, smashing fingers or limbs, labor pains, etc. Acute pain is most often a symptom of injured or diseased tissue – as it heals, the pain would normally recede. The medical treatment, thereby focuses on healing the underlying causes, such as torn muscles, etc. The longer and more intense the pain becomes, the more likely it will become a less acute pain and a more likely chronic pain, which then requires more analysis and often more proactive and long-term medical assistance.

Chronic pain

Chronic pain, in most instances is considered a disease state – it has outlasted the normal time of healing associated with an initial injury and therefore it is often hard to diagnose where it has come from and whether it will have a defined end point. This is pain that lasts longer than 6 months. For all these reasons, the diagnosis behind chronic pain may take more time and is more complex, relying on a multidisciplinary approach.

In chronic pain, the nervous system may be sending a pain signal even though there is no ongoing tissue damage. The nervous system itself misfires and creates the pain. In such cases, the pain is the disease rather than a symptom of an injury. Long-term sicknesses that could result in chronic pain include multiple sclerosis, inflammatory disease such as rheumatoid arthritis, fibromyalgia, degenerative diseases like osteoporosis or osteoarthritis, and cancer.

Continuing conditions that may be the reason for chronic pain include peripheral neuropathy such as carpal tunnel syndrome, sinus headaches, migraine, and ear infections. Initial injuries like a sprain, along with back pain, heel pain, sciatica, and Achilles tendonitis may also become chronic. This pain is certainly much less understood than acute pain, partly due to its complexity.

Capital Pain Institute

At Capitol Pain Institute, we work with you to determine what type of pain you are dealing with and how we can help you create a pain management plan. Dr. Matthew Schocket founded the Capitol Pain Institute to provide progressive and innovative pain management in Austin and central Texas.

The patient experience here at the Capitol Pain Institute begins with a face-to-face consultation with one of our pain management physicians.  During this initial visit, a unique treatment plan is designed based on the specific individual needs of each patient. Your role in this plan is vital as it has to fit you and your needs. With our multidisciplinary approach, we are able to look at rehabilitation programs, psychological therapy, and physical therapy in order to offer you a comprehensive treatment plan. For more information or to arrange a consultation, contact us at help@capitolpain.com.

Patient Testimonial – “Filtered” Yelp Reviews

Since Yelp has decided to filter our reviews, we have decided to post their filtered reviews to our website so that everyone can decide for themselves which reviews are useful (instead of Yelp doing it for you).  These reviews are copied and pasted directly from the Yelp “not-recommended” page.

  • 60s Patient Testimonial   Filtered Yelp Reviews
    • L W.
    • Austin, TX
    • 0 friends
    • 18 reviews

    7/30/2014

    I have been a patient of Dr. Schocket and Capitol Pain Institute for almost three years now. Before that, I suffered with terrible pain, neuropathy and restless leg syndrome my entire life. Exhausting every recommended medicine available and every general practitioner left me hopeless and tired. After being referred to Dr. Schocket, I was immediately taken in, evaluated and treated. He is a caring doctor and very knowledgeable about a wide-range of medications and treatments. It wasn’t long after my initial appointment with Dr. Schocket that I finally found relief with a combination of effective medication. Each time I visit, I’m treated with the utmost concern. I love CPI so much, that I actually commute from Cypress after we moved because I’m unwilling to give up Dr. Schocket’s expertise and his practice. The only negative thing I could say would be the long wait times, but within the last 6 months, CPI has relaunched their scheduling program and I’ve been in and out each time in 30 minutes or less. CPI is nothing close to being a pill-mill or some kind of junkie pharmacy like some of the other reviews claim. They’ve been crystal clear about the law and what’s allowed and expected of us as patients from Day One. There’s nothing lax, or unprofessional about it. I highly recommend CPI and Dr. Schocket to anyone frustrated with chronic pain!

     

EMG & NCS: What do all these letters mean to the patient?

EMG & NCS: What do all these letters mean to the patient?

EMG & NCS. At first glance, the name of this study can easily confuse a patient. However, once it is broken down into its components, the words explain themselves. Electro-myo-graphy and Nerve Conduction Studies are, as the names state, electrical studies of the muscle “myo” and nerves. In a normal muscle, the electrical signal or waveform that is produced has a certain onset or latency, size or amplitude, duration, appearance, and sound. In muscles innervated by damaged nerves, the latency of the nerve may be delayed, amplitude may be abnormally large or small, and the clinician may hear certain sounds produced which indicate acute or chronic damage.

During the day-to-day routine in the clinical setting, we try to determine if a patient would benefit from an EMG/NCS through the process outlined below.

On our first evaluation of a patient, he or she may report numbness or tingling in one, two or all extremities with or without any pain complaints. At this point, the clinician should inquire about the duration of the patient’s symptoms, and exactly what areas are affected by the symptoms. Some of these questions may include:

  • What time of day are symptoms present?
  • Is the numbness and tingling worse at night or early mornings?
  • Is the numbness and tingling related to certain activities?
  • Are there any medications which alleviate the symptoms?

 

After obtaining the appropriate initial history, it is essential to review the patient’s medical history, as certain medical conditions can cause neuropathy affecting the sensory function of the nerves (which allow the patient to feel certain sensations). These medical conditions include diabetes, hypothyroidism, connective tissue disease, and alcohol consumption, among several others.

A thorough history is often followed by a physical examination of the patient, during which the clinician will focus on range of motion, muscle strength, muscle atrophy, and changes in sensation.

Once the determination is made that a patient has a clinical picture consistent with possible nerve damage, the EMG/NCS study is scheduled. The test generally starts with the NCS, or nerve conduction studies portion and involves the patient lying flat on a comfortable table. Then, grounding and recording wires, which are attached to gel-covered stickers, are placed directly on the skin. Therefore, it is essential that the patient does not apply any lotions or oils to the area to be tested. An electrical stimulator is applied to the skin, and then the patient feels a tingling sensation. Subsequently, a waveform is recorded from the particular nerve being tested, for the clinician to view and evaluate.

The second portion of the exam is the EMG, or electromyography, and focuses on testing the electrical activity of the muscle. A small, acupuncture sized needle is inserted into a particular muscle, and the clinician evaluates the size, shape, and sound of the signal. Based on the results of this evaluation, the clinician can diagnose a nerve problem in the arms, legs, or spine.

In summary, EMG & NCS is useful in the diagnosis of several conditions. Some of these include compressed nerves in the arms or legs (eg. Carpal Tunnel Syndrome or Tarsal Tunnel Syndrome), peripheral neuropathy (eg. Diabetic Neuropathy), and pinched nerves in the neck and back (radiculopathy). As with any diagnostic study, the findings of an EMG/NCS should be incorporated into the patient’s entire clinical picture.

Watch the video below to know what to expect during your EMG & NCS test.

Back Pain: Spondylosis, Spondylolysis, and Spondylolisthesis

Have you read your MRI report recently and ended up more confused about your low back pain than before you began? If so, you are not alone.  The medical terms for low back problems confuse many medical professionals who don’t deal with these issues on a regular basis.  The purpose of this post is to help explain what is going on with your back, so that you can make a more informed decision on which treatments to choose.

The 3 main terms we are going to discuss are spondylosis, spondylolysis, and spondylolisthesis.  Each is defined below and a general discussion of treatment options follows.

Spondylosis refers to degenerative osteoarthritis of the spine – essentially the space between adjacent spinal vertebrae narrows. Because this condition commonly occurs in the zygapophysial (facet) joints or the intervertebral discs, it is often referred to as facet syndrome or degenerative disc disease.

Spondylolysis is a defect of a vertebra in the pars interarticularis – most typically a stress fracture that is caused by repetitive trauma done to the lumbar spine from strenuous sports such as football, weightlifting, cheerleading, or gymnastics.  Spondylolysis is also linked to certain inherited spinal anatomy (increased size and shape of the L4 superior articular process).

Spondylolisthesis is the displacement of a vertebra, most commonly occurring after a break or fracture.  There are 2 common forms of spondylolisthesis.

Isthmic (spondylolytic) spondylolisthesis is the most common form, with a reported prevalence of 5–7 percent in the US population. It usually progresses from spondylolysis over time.

Degenerative spondylolisthesis develops as a long-term result of progressive spondylosis. Facet arthritis and ligamentum flavum weakness may result in slippage of a vertebrae. Degenerative forms are more likely to occur in women, persons older than fifty, and African-Americans.

Symptoms:

Spondylosis, spondylolysis, or spondylolisthesis can cause stiffness and pain in the spine (lower back pain or neck pain), however, when severe, the narrowing may cause pressure or compression of the nerve roots.  Compression of a nerve root emerging from the spinal cord may result in radiculopathy (sensory disturbances, such as severe pain, weakness, or tingling in the neck, shoulder, arm, back, and/or leg, possibly accompanied by muscle weakness).

Treatments:

Treatment begins with conservative therapy including: physical therapy (including yoga and pilates), anti-inflammatory medications, epidural steroid injections, facet joint injections, radiofrequency ablation, massage therapy, acupuncture, and chiropractic care.  Often a back brace will help patients, especially those with spondylolisthesis to perform certain activities with less pain.

If there is nerve root irritation or nerve root compression causing radiculopathy that is not improved with conservative care, decompression surgery may be very effective in relieving the pain.  Fusion surgery is a poor option for the treatment of spondylosis, but may be considered for severe cases of spondylolisthesis.

Regenerative medicine has recently emerged for spondylosis and spondylolysis.  There are several reports of long-term successful treatment of low back pain with both PRP (platelet rich plasma) therapy or stem cell treatments.

For those interested, I have included a video with some excellent exercises for low back pain.

Fast facts: Are you at an Increased Risk for Back Pain?

An important question that is frequently put to our back pain management specialists here at the Capitol Pain Institute is whether there are certain jobs or lifestyles that increase the risk of back pain. The simple answer to this question is that it is not professions or lifestyles that influence back pain probability, but due to a wide specter of reasons. Statistics show that most adults would, at one time or another during their lifetime, experience a severe case of back pain, especially lower back pain. There is even evidence to show that a quarter of Americans may have a relapse of severe back pain once a quarter. These people come from different creeds, have different day-to-day routines and so forth, yet are united by this worrying statistic. Suffice it to say that back pain leads to more work missed than any other occupational disability.

Why does back pain occur?

Back Pain 225x300 Fast facts: Are you at an Increased Risk for Back Pain?As mentioned before, there are plenty of factors that can influence the appearance of back pain. There is the excessive strain put on muscles and ligaments, injury due to a car accident or workplace incident, nerve irritation and so on and so forth. A key point to remember about back pain is that it is not always a manifestation of something wrong with the back per se, as back pain can be a direct manifestation and symptom of other health issues. Back pain in itself is a very broad term that includes both the symptoms of various injuries and the elements of deeper health concerns. Neck and back strain, unusual physical activity, direct and indirect injury, shock, uncomfortable posture can all contribute to the formation of back pain.

What causes increased risk of back pain?

The non-exhaustive list above should provide some direction in terms of activities and occupations that may be closely linked with greater risk of back pain. There are, of course, ways to try and avoid this back pain. Our back pain doctor in Austin at the Capitol Pain Institute recommend abstaining from physical activity that is not at par with your usual level of strain on your muscles and ligaments. They also recommend taking it slow when pain does occur, as forcing yourself past the mild irritating pain can lead to much greater consequences. What our doctors stress, however, is that it is usually very difficult to pinpoint the exact reasons for a particular back pain incident. Given the interconnectivity and complexity of the human nervous system, most of the time no one factor can be attributed to increased back pain risk. Nerve entrapment, muscular injury, herniated disks, joint erosion are all named as possible causes of back pain, but caution is urged when trying to link the condition to just one of the aforementioned issues.

How we can help

No online chat or discussion can substantiate a visit to meet with our trained medical professionals in person. Diagnosis should never be given out online, and the materials you would find here are for informational purposes only, thus we encourage you to contact our doctors at the Capitol Pain Institute today to book an up and personal review of your individual situation.

Understanding Spine Basics: The Vertebrae, Discs and the Spinal Cord

Dealing with back pain is torture, but the more you know about spine basics, such as the vertebrae, discs and the spinal cord, the better you will understand your pain. Although it won’t lessen it, it can help you avoid making the situation worse.

A lot of strain is put on your spine; after all it is what holds up the heads, shoulders, and the entire body. It is the frame that supports your body and allows you to twist and bend. It also acts to protect your spinal cord by encasing it.

Understanding Spine Basics: The Vertebrae, Discs and the Spinal Cord

 To get a better understanding of your spine, let’s break down the components that hold it together.

Spine Basics – The Vertebrae

You have probably heard of “vertebrae”, which is the plural of vertebra, but do you have a firm understanding of what they are?

The vertebrae are the 33 individual interlinked bones that form your spinal column. They are broken down into five main groups that depend on where they are located on the backbone.

  • The base of your skull has 7 cervical vertebrae
  • 12 thoracic vertebrae in your upper back
  • 5 lumbar vertebrae in your lower back, below the curve.
  • Below your lower back are 5 vertebrae that are fused together to form the sacrum, which is part of your pelvis.
  • The last 4 vertebrae are fused together to make your tailbone.

The vertebrae in each region have unique features that help them execute their main functions.

Spine Basics – Discs                  

 Between each vertebra is what are medically called intervertebral discs, but are usually shorted to “discs”. The discs in your back Spine Basics 268x300 Understanding Spine Basics: The Vertebrae, Discs and the Spinal Cordconnect each vertebra to the next. They’re flat and round with a gel-like center, and are about a half an inch thick.

Discs are made of two components:

  • Nucleus pulposus: Is similar to jelly, and comprises the center of your disk
  • Annulus fibrosus: The flexible outer-ring of the disk, which consists of several layers similar to elastic bands and resembles the cross-section of an onion.

Discs are located in front of your spine, and are what give the torso the ability to move forwards, backwards, side to side, and rotate. They are also responsible for absorbing shock and pressure during activities such as running, walking and even sitting.

Spine Basics – The Spinal Cord

 Your spinal cord goes from your skull down to your lower back, and goes through the middle section of each vertebra. Nerves flow from your spinal cord to every muscle in your body, via openings in your vertebrae (foramen), and carry messages between your brain and muscles. Because of this anatomical set-up, injury or damage to your spinal cord can result in serious problems in other areas of your body including your limbs, muscles, skin and organs. Since your spinal cord is protected by vertebrae, disks, ligaments and muscles, you also have to be careful when you injure these areas of your back.

 Now you know the basics of your spine, its components, and also how they work together. If you’re dealing with back pain and want to know how our Austin pain doctors at the Capitol Pain Institute can help you, contact us by e-mail at help@capitolpain.com or call us at (512) 467-7246.

When is a Migraine headache really a Migraine?

When is a Migraine headache really a Migraine?

“My head hurts…It must be a migraine!” Is a common complaint amongst many patients in neurology clinics and Austin pain clinics alike. However, not all headaches have the same triggers, causes, or treatments. In specific, a migraine is a severe headache that may be commonly associated with nausea and/or light and sound sensitivity. This type of headache is distinctly different from cluster type headaches (pain behind the eye) and tension type headaches (pain across forehead) which may be discussed in more detail with your physician.

So when is a “migraine” really a migraine headache? The once popular ‘vascular theory of migraine’ purported that migraine headaches were a cause of dilatation and vasoconstriction of cerebral blood vessels is no longer considered mainstream [1-3]. More reflective of current research is the idea that migraines are caused by ‘cortical spreading depression’ or a wave of electrical activity sweeping across the brain.

This electrical wave activates a nerve system known as the ‘trigeminovascular system’ (TVS) which is a network of nerves that can irritate the pain-sensitive lining of the brain (the meninges). The TVS explains the distribution of migraine pain, which often includes the front and back of the head and the upper neck [4,5].The prolongation and intensification of migraine pain is propagated by the inflammatory response (neurogenic inflammation) triggered by the TVS [6].

What role does genetics have with migraine headaches? Migraine headaches are in most instances inherited. Subtle abnormalities, involving membrane channels, receptor families, and enzyme systems have been linked to migraine in certain groups and individuals. The importance of inheritance in migraine has long been recognized [7]. One early general population based study found that the risk of migraine in relatives of migraineurs was three times greater than that of relatives of non-migraine control subjects [8].

How common are migraine headaches? Migraine is a common disorder that affects up to 12 percent of the general population [8]. It is more frequent in women than in men, with attacks occurring in up to 17 percent of women and 6 percent of men each year [9,10]. Migraine is most common in those aged 30 to 39, an age span in which prevalence in men and women reaches 7 and 24 percent, respectively [10]. Migraine also tends to run in families. Migraine without aura is the most common type, accounting for approximately 75 percent of cases.

What is a migraine aura? About 25 percent of people with migraines experience one or more focal neurologic symptoms called the migraine aura. Auras are most often visual, but can also be sensory, verbal, or motor disturbances. Visual auras may either appear as a bright spot or as an area of visual loss or geometric shapes and zigzagging lines may often appear. [12]. Less common than the visual and sensory auras, is the language or dysphasic aura that causes transient language problems that may run the gamut from mild wording difficulties to frank difficult speaking [13]. Traditional teaching is that migraine aura usually precedes the headache [13]. However, prospective data suggest that most patients with migraine experience headache during the aura phase [14]. It may also occur without an associated headache.

Can I feel a migraine starting? A migraine prodrome (forewarning) occurs in up to 60 percent of people 24 to 48 hours prior to the onset of headache i.e. euphoria, depression, irritability, food cravings, constipation, neck stiffness, and increased yawning [10].

How does a migraine progress? Migraine is a disorder of recurrent attacks. The attacks unfold through a cascade of events that occur over the course of several hours to days. A typical migraine attack progresses through four phases: the prodrome, the aura, the headache, and the postdrome [11]. The headache of migraine is often but not always unilateral and tends to have a throbbing or pulsatile quality, especially as the intensity increases. As the attack severity increases over the course of one to several hours, patients frequently experience nausea and sometimes vomiting. Many individuals report sensitivity to light or sound during attacks, leading such migraine sufferers to seek relief by lying down in a darkened, quiet room.

What is a migraine postdrome — Once the spontaneous throbbing of the headache resolves, the patient may experience a postdromal phase, during which sudden head movement transiently causes pain in the location of the headache. During the postdrome, patients often feel drained or exhausted.

What precipitates or exacerbates a migraine? An evidence-based review concluded that stress, menstruation, visual stimuli, weather changes, nitrates, fasting, and wine were probable migraine trigger factors, while sleep disturbances and aspartame were possible migraine triggers [15]. All of the probable and possible migraine triggers except aspartame were also general headache triggers.

In a retrospective study of 1750 patients with migraine, approximately 75 percent reported at least one trigger of acute migraine attacks [16]. In order of descending frequency these included:

  • Emotional stress (80 percent)
  • Hormones in women (65 percent)
  • Not eating (57 percent)
  • Weather (53 percent)
  • Sleep disturbances (50 percent)
  • Odors (44 percent)
  • Neck pain (38 percent)
  • Lights (38 percent)
  • Alcohol (38 percent)
  • Smoke (36 percent)
  • Sleeping late (32 percent)
  • Heat (30 percent)
  • Food (27 percent)
  • Exercise (22 percent)
  • Sexual activity (5 percent)

Obesity has been associated with an increased frequency and severity of migraine [17-20].

Are there ways I can tell a tension headache from a migraine headache? While the features of migraine and tension headache overlap, the clinical features that appear to be most predictive of migraine include nausea, sensitivity to light, sensitivity to sound, and worsening of symptoms by physical activity [21, 22]. Food triggers are also more common with migraine than tension-type headache.

The International Headache Society (IHS) diagnostic criteria for migraine with and without aura are as follows [14]:

Migraine without aura — Migraine without aura is a recurrent headache disorder that fulfills the following criteria [14]:

  • Headache attacks last 4 to 72 hours
  • Headache has at least two of the following characteristics: unilateral location; pulsating quality; moderate or severe intensity; aggravation by routine physical activity
  • During headache at least one of the following occurs: nausea and/or vomiting; photophobia and phonophobia
  • At least five attacks occur fulfilling the above criteria
  • History, physical examination, and neurologic examination do not suggest any underlying organic disease

Migraine with aura — In migraine with aura, attacks include the transient appearance of focal neurologic symptoms that usually develop gradually over 5 to 20 minutes and last for less than 60 minutes. A headache that has the features of migraine without aura begins during the aura or follows the aura within 60 minutes.

Although too detailed for this overview, it is important to know that other types of migraines exist, including ‘Menstural migraines’  (a migraine headache that occurs in close temporal relationship to the onset of menstruation), ‘Basilar-type migraine’ (often present as difficulty speaking, ear ringing, double vision, decreased hearing then followed by a typical migraine headache), etc.

The purpose of this overview is for informational purposes only not as a tool for diagnosis, treatment, or management. If you experience any types of head pain, visual disturbances, nausea and vomiting it is imperative that you seek immediate consultation with a physician for treatment as many other diseases or injuries can cause similar signs and symptoms and may be life threatening. Consult with your physician regarding diagnosis, management, and prevention.

 

REFERENCES

  1. Charles A. Advances in the basic and clinical science of migraine. Ann Neurol 2009; 65:491.
  2. Charles A. Vasodilation out of the picture as a cause of migraine headache. Lancet Neurol 2013; 12:419.
  3. Amin FM, Asghar MS, Hougaard A, et al. Magnetic resonance angiography of intracranial and extracranial arteries in patients with spontaneous migraine without aura: a cross-sectional study. Lancet Neurol 2013; 12:454.
  4. Sessle BJ, Hu JW, Dubner R, Lucier GE. Functional properties of neurons in cat trigeminal subnucleus caudalis (medullary dorsal horn). II. Modulation of responses to noxious and nonnoxious stimuli by periaqueductal gray, nucleus raphe magnus, cerebral cortex, and afferent influences, and effect of naloxone. J Neurophysiol 1981; 45:193.
  5. Wise SP, Jones EG. Cells of origin and terminal distribution of descending projections of the rat somatic sensory cortex. J Comp Neurol 1977; 175:129.
  6. Sarchielli P, Alberti A, Floridi A, Gallai V. Levels of nerve growth factor in cerebrospinal fluid of chronic daily headache patients. Neurology 2001; 57:132.
  7. Lance JW, Anthony M. Some clinical aspects of migraine. A prospective survey of 500 patients. Arch Neurol 1966; 15:356.
  8. Merikangas KR, Risch NJ, Merikangas JR, et al. Migraine and depression: association and familial transmission. J Psychiatr Res 1988; 22:119.
  9. Lipton RB, Stewart WF, Diamond S, et al. Prevalence and burden of migraine in the United States: data from the American Migraine Study II. Headache 2001; 41:646.
  10. Stewart WF, Shechter A, Rasmussen BK. Migraine prevalence. A review of population-based studies. Neurology 1994; 44:S17.
  11. Lipton RB, Bigal ME, Diamond M, et al. Migraine prevalence, disease burden, and the need for preventive therapy. Neurology 2007; 68:343.
  12. Charles A. The evolution of a migraine attack – a review of recent evidence. Headache 2013; 53:413.
  13. Kelman L. The premonitory symptoms (prodrome): a tertiary care study of 893 migraineurs. Headache 2004; 44:865.
  14. Cutrer FM, Huerter K. Migraine aura. Neurologist 2007; 13:118.
  15. Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders: 2nd edition. Cephalalgia 2004; 24 Suppl 1:9.
  16. Hansen JM, Lipton RB, Dodick DW, et al. Migraine headache is present in the aura phase: a prospective study. Neurology 2012; 79:2044.
  17. Martin VT, Behbehani MM. Toward a rational understanding of migraine trigger factors. Med Clin North Am 2001; 85:911.
  18. Kelman L. The triggers or precipitants of the acute migraine attack. Cephalalgia 2007; 27:394.
  19. Bigal ME, Liberman JN, Lipton RB. Obesity and migraine: a population study. Neurology 2006; 66:545.
  20. Bigal ME, Lipton RB. Obesity is a risk factor for transformed migraine but not chronic tension-type headache. Neurology 2006; 67:252.
  21. Bigal ME, Tsang A, Loder E, et al. Body mass index and episodic headaches: a population-based study. Arch Intern Med 2007; 167:1964.
  22. Smetana GW. The diagnostic value of historical features in primary headache syndromes: a comprehensive review. Arch Intern Med 2000; 160:2729.

New Diagnostic Criteria for Fibromyalgia

The Hunt for the Correct Diagnosis: Fibromyalgia vs Myofascial Pain Syndrome

A Glance at the Latest Breakthroughs in Diagnosis and Treatment

Although hard to believe, there was a time when Fibromyalgia was treated as a “catch all diagnosis” or a diagnosis applied to any patient in diffuse, widespread chronic pain without a clear cause. As there was no initial diagnostic criteria, and the condition was poorly understood, many patients would be mislabeled with the diagnosis of “Fibromyalgia” without a clear understanding of why or how this diagnosis was reached. Fortunately, there has been a great deal of headway in defining Fibromyalgia, learning about its cause, and separating this diagnosis from other similar pain conditions.

Fibromyalgia is regarded as a chronic condition that causes intense pain all over the body as well as causes a range of other symptoms. Doctors have classified Fibromyalgia as a syndrome, which means it is comprised of signs, symptoms, and characteristics that often go hand-in-hand. A few commonly reported characteristics include “hurting all over,” “feeling exhausted,” morning stiffness, poor or un-refreshing sleep, memory impairment, and abdominal cramps.  See the Centers for Disease Control Fact Sheet on Fibromyalgia.

The term Fibromyalgia was coined circa 1976. However, it wasn’t until 1990 that the American College of Rheumatology published the first diagnostic criteria. Historically, a patient was diagnosed with Fibromyalgia once other syndromes were ruled out, and was founded upon “tender points.” These tender points needed to be on both sides of the body, above and below the waist in 11 of 18 specific spots on the body (as the diagram below demonstrates). These tender points needed to persist for at least 3 months. A new paradigm in diagnosing Fibromyalgia has stirred the medical community in recent years and caught everyone’s attention – patients and physicians alike. The Widespread Pain Index (WPI) and the Symptoms Severity Scale Score (SS) were recently introduced as two novel methods of assessing for Fibromyalgia. In essence, a diagnosis of Fibromyalgia may be reached under this new paradigm via a minimum score combination of the WPI and SS.

The medical community’s understanding of fibromyalgia has not only led to novel methods of diagnosis, but also in treatment and understanding of cause. The current thought is that Fibromyalgia represents a ‘malfunction’ of the central nervous system or a ‘central sensitization’ so to speak. In other words, those stimuli that would be interpreted by the brain and spinal cord as “mildly unpleasant” may be misinterpreted or increased in amplitude to “very unpleasant / painful.” This amped up neural circuitry may explain why patients not only may feel pain throughout their body but also why it may affect many other body systems including the gastrointestinal tract and cognitive functioning. This forward progress is in-line with the FDA approving three drugs in the treatment of Fibromyalgia (Lyrica, Cymbalta, and Savella) all with direction action on the central nervous system and more focused research into future potential therapies. Moreover, improved sleep habits, regular exercise, and stress reduction are also regarded as beneficial for this condition.

Fibromyalgia should not be confused with Myofascial Pain Syndrome. Understanding the differences between these commonly confused conditions not only helps direct targeted therapy but reduces misdiagnosis.  Unlike the symmetric “tender points” once touted in Fibromyalgia, Myofascial pain syndrome is hallmarked by “trigger points” or focal, painful, taut muscle bands that may be felt on the physical exam.  These tender points or “knots” can be painful, especially when under direct pressure and may result from tissue trauma, inflammation/irritation, or stress. Others speculate these taut muscle bands represent regions of reduced blood flow. Patients with these trigger points may experience pain at these sites or referred pain resulting in headaches, poor sleep, or decreased range of motion in joints. The treatment for Myofascial Pain Syndrome is commonly regarded as physical therapy, medications including NSAIDs and tricyclic antidepressants, and trigger point injections which increase regional blood flow and decrease inflammation through the deposition of local anesthetic and steroids in these regions. Ultrasound guidance has allowed for enhanced safety and efficacy of these injections.

At Capitol Pain Institute, our expert Austin pain doctors are aware of nuances in these pain conditions, the latest diagnostic criteria, therapeutic modalities, and medications to treat each of these pain conditions. We invite you to engage our physicians and nurse practitioners to speak more about your pain condition and how we may be of help!