Courage in pain or adversity: “she endured her illness with great fortitude”.

I was writing an email to my father and out popped the word “fortitude”.  “Wish I had the fortitude” I wrote.  I know what it means but I looked it up anyway. Its definition pops out AT ME.  (see above)  And I can’t help thinking it’s not a coincidence.  I’m not enduring my illness with any for·ti·tude  at all and I should be.  I am more of an unorganized mess-lately hit with that dreaded brain fog forgetting what I’m doing and what I’m saying, names, places, faces, details.  Not enough of a help to my family.  I need to step up higher.  My husband is tired.  My son needs my help. 

Disability hearing is coming up in September.  The board of education kicked back my dismissed Sallie Mae school loans because my GP is a DO.  Go figure.  Alot going on and alot coming up.  My foot surgery seems failed and I will likely need two more, one to kill the other side of the nerve and one to take the toe.  The familiar pain has returned along with my unsettledness & has run off with my for·ti·tude.

Tomorrow is another day.  Tally Ho!


The EYES Have It! Uveitis, that is!

ps.  Does the inflammation highway ever run out of track?  I don’t think so!  Todays stop boys and girls will be recurring anterior uveitis.  You-vee itis?  Me-vee-itis?  We all you-me-itis!

This is my second round of pretty bad uveitis-bad enough for the men in white to give me an iv of steroids and a shot in the eyes of the same.  YES, I said a Shot In The Eyes.

My last bout-December 2012 came accompanied with sacroiliitis, alias inflammatory arthritis, alias “are you kidding me” kind of pain.  So far it’s starting about the same.  While uveitis can come to the inflammation party on its own-there are alot of conditions that also can cause it.  In my case docs just blamed the L-Word although my grandmother had ankylosing spondylitis-and she may have set a genetic trap for me.  lol.  There’s a genetic marker-it is called HLA-B27 tissue type and testing is appropriate if you have both sacroiliitis and chronic recurring anterior uveitis.

Here’s what to look for in the inflammation of the eye:  uveitispic

And here’s my eyejulierighteye julieseyejuly29s:  juliejuly 'juliemalarjuly2013 juliemalarjuly2013 2 Of course the uveitis highjacked a malar rash and low grade fever  on it’s way to rain on my surgery recovery parade.  Just when I thought it was safe to start dibbling and dabbling with projects and posts.  It’s getting better now by leaps and bounds thanks to the evil but wonderful prednisone and steroid drops.  All the white floaters are gone (I CAN SEE AGAIN) and the pressure and inflammatory pain is down!  Yippeee!  I don’t know about you-but lupus might be the great imitator-however I am the great procrastinator-and that trumps lupus.  😉

Here is some info about Uveitis (there is more than one kind) and also while playing around I found a new medicine in trial stages for eye inflammation.  This is potentially sight-saving.  And unfortunately-once lupus stops at the door of the eyes, it comes back often to the party.


The signs, symptoms and characteristics of uveitis include:

  • Eye redness
  • Eye pain
  • Light sensitivity
  • Blurred vision
  • Dark, floating spots in your field of vision (floaters)
  • Decreased vision
  • Whitish area (hypopyon) inside the eye in front of the lower part of the colored area of the eye (iris)

The site of uveitis varies and is described by where in the eye it occurs.

  • Anterior uveitis affects the front of your eye (also called iritis).
  • Posterior uveitis affects the back of your eye (also called choroiditis).
  • Intermediary uveitis affects the ciliary body (also called cyclitis).
  • Panuveitis occurs when all layers of the uvea are inflamed.

In any of these conditions, the jelly-like material in the center of your eye (vitreous) can also become inflamed and infiltrated with inflammatory cells.

Symptoms may occur suddenly and get worse quickly, though in some cases, symptoms develop gradually. Symptoms may be noticeable in one or both eyes.

When to see a doctor
Contact your doctor if you think you may have symptoms of uveitis. Your doctor may refer you to an eye specialist (ophthalmologist). If you’re having significant eye pain and new vision problems, seek prompt medical attention.

If uveitis is caused by an underlying condition, treatment will focus on that specific condition. The goal of treatment is to reduce the inflammation in your eye.

Treatment of uveitis may include:

  • Anti-inflammatory medication. Your doctor may prescribe anti-inflammatory medication, such as a corticosteroid, to treat your uveitis. This medication may be given as eyedrops. Or, you may be given corticosteroid pills or an injection into the eye. For people with difficult-to-treat posterior uveitis, a device that’s implanted in your eye may be an option. This device slowly releases corticosteroid medication into your eye for about 2 1/2 years.
  • Antibiotic or antiviral medication. If uveitis is caused by an infection, antibiotics, antiviral medications or other medicines may be given with or without corticosteroids to bring the infection under control.
  • Immunosuppressive or cell-destroying (cytotoxic) medication. Immunosuppressive or cytotoxic agents may be necessary if your uveitis doesn’t respond well to corticosteroids or becomes severe enough to threaten your vision.
  • Surgery. Vitrectomy — surgery to remove some of the jelly-like material in your eye (vitreous) — may be necessary both for diagnosis and management of your uveitis. A small sample of the vitreous can help identify a specific cause of eye inflammation, such as a virus, bacterium or lymphoma. The procedure may also be used to remove developing scar tissue in the vitreous.

The part of your eye affected by uveitis — either the front (anterior) or back (posterior) of the uvea — may determine how quickly your eye heals. Uveitis affecting the back of your eye tends to heal more slowly than uveitis in the front of the eye. Severe inflammation takes longer to clear up than mild inflammation does.

Uveitis can come back. Make an appointment with your doctor if any of your symptoms reappear after successful treatment.

Eye Disease: Preliminary Findings On Uveitis Drug

Aug. 22, 2012 — Shree Kurup, M.D., director of research in the ophthalmology department at Wake Forest Baptist Medical Center, will present the preliminary findings of a Phase 3 clinical trial on a new drug for the treatment of uveitis, a serious inflammatory condition of the uvea, the middle layer of the eye that provides most of the blood supply to the retina.

Link to Clinical Trials for NEW uveitis medication! 

L for LUPUS, N for Neurectomy & No More Toe Pain???

juliehospitalI had what is called a median nerve neurectomy.  My orthopedic surgeon snipped the median nerve in my right foot that leads to the bottom of the fourth toe (on the left side of the toe) with the hopes and intentions of killing the nerve dead!  That toe has certainly been the bane of my existence for the last five years.  Sometimes something so small can turn into something so big and painful.  They call it a Morton’s Neuroma.  Likely mine was caused by inflammation in the connective tissue of my feet-plantar fasciitis.  At one time my PF was so bad I couldn’t walk.  Cortisone shots right into the plantar gave me back my mobility but the shots into that toe and median nerve stopped working and the zapping and stinging and sharp pains continued.

I was lucky.  I found an orthopedic surgeon that specializes in FEET.  He went in through the top of the foot and snipped the median nerve right down the middle to the back of the fourth toe right foot.  Here’s a better explanation of what a Morton’s Neuroma is and a short video animation I found.

Lupus is different in every patient.  Mine likes to attack my peripheral and cranial nerves, skin and blood.  This is just one example of what lupus can do.


Morton’s Neuroma is a painful condition of the forefoot that is caused by the entrapment of the common intermetatarsal nerve as it passes through the forefoot to the toes. This condition was first described by Dr. Morton, a Viennese physician, in 1876. The most common location for Morton’s neuroma is between the third and fourth toes. The second most common location is between the second and third toes.

To help understand this condition a bit better, let’s break down the word neuroma into its’ root form. Neuro relates to the nervous system and in this case, we are describing a portion of the peripheral nervous system. The suffix ‘oma’ is the Latin term that defines a tumor or swelling that is of primary origin. Put the terms together and what is described is a tumor or swelling of a peripheral nerve. Interestingly, a Morton’s neuroma is not truly a tumor, but more accurately, a nerve entrapment. Although the term neuroma is somewhat inaccurate in describing this condition, the term neuroma is still used today to describe this unique nerve entrapment.  Other terms may be used to describe Morton’s neuroma.  These terms include intermetatarsal neuroma, Morton’s metatarsalgia, Morton’s neuralgia, plantar neuroma, intermetatarsal perineural fibroma or intermetatarsal nerve entrapment.

What causes Morton’s Neuroma? Why does the intermetatarsal nerve become entrapped? Clinicians and surgeons recognize a number of factors that may aggravate Morton’s neuroma, but the primary cause of Morton’s neuroma remains elusive. Shoes that are tight in the forefoot will contribute to the symptoms of Morton’s Neuroma by binding the forefoot and compressing the common intermetatarsal nerve. High heels will also act to increase the ground reactive forces. Ground reactive force is the amount of force generated as the foot pushes against a fixed surface like the floor. With high heels, the amount and focus of ground reactive force increases since weight bearing is focused in a smaller area (just the forefoot). A higher heel also puts the common intermetatarsal nerve under tension, making it more prone to injury. Activities such as squatting will increase the ground reactive force applied to the plantar foot and aggravate the symptoms of Morton’s neuroma. And finally, clinician also agree that hypermobility of the forefoot can contribute to the formation of Morton’s neuroma.

Treatment of Morton’s neuroma

It’s interesting to note that until the early 1990’s, we treated Morton’s neuroma in same way as described by Dr. Morton some 100 years ago. But over the past ten years, our understanding and treatment of neuromas has changed dramatically. Our understanding of Morton’s neuroma as an entrapment and not a tumor can be attributed to the work of Steve Barrett, DPM. Dr. Barrett was the first to take a critical look at Morton’s neuroma and describe it as an entrapment rather than a tumor.

What Dr. Barrett recognized was that the common intermetatarsal nerve is sometimes prone to becoming entrapped as it passes beneath the intermetatarsal ligament. This was a new concept for us in light of the fact that we had considered Morton’s neuroma a tumor. In fact, Dr. Barrett’s findings enabled us to recognize Morton’s Neuroma to be similar to other nerve entrapments such as carpal tunnel syndrome or tarsal tunnel syndrome. Subsequently, the treatment of Morton’s Neuroma has been slowly changing over the last ten years as the result of a new endoscopic surgical procedure first described by Dr. Barrett.

Diagnostic testing to evaluate Morton’s neuroma includes plain x-rays, diagnostic ultrasound and MRI. Plain x-rays are not actually used to visualize the nerve, but are use rather to screen for bone and joint pathology adjacent to the nerve. Metatarsal fractures, Freiberg’s infraction and osteoarthritis are common conditions that can influence the behavior of Morton’s neuroma and need to be evaluated with x-ray.

Several authors have suggested that the efficacy of MRI and ultrasound as diagnostic tools are comparable when evaluating patients for Morton’s neuroma. Diagnostic ultrasound is significantly less expensive and much more readily available compared to MRI. Kankanala et. al described a 91.48% pre-op predictive value for diagnostic ultrasound when screening for Morton’s neuroma.

Conservative care of Morton’s neuroma can be quite successful. 70% or more of new Morton’s neuroma patients respond to simple changes in shoes such as a wider toe box. Shoe padding can also help treat Morton’s neuroma. Metatarsal pads are an important tool for patients with Morton’s neuroma symptoms. A metatarsal pad is a small lift that is positioned in the shoe just proximal (behind) the weight bearing surface of the metatarsal bones. A metatarsal pad lifts and separates the metatarsal bones thereby decreasing the pressure on the intermetatarsal nerve. Some prefabricated arch supports come with a metatarsal pad already seated in the correct position. Using inserts with a metatarsal pad is sometimes the easier way to use a met pad because they can be easily moved from shoe to shoe. Also, by using an insert with a fixed metatarsal pad, the position of the met pad is always in the correct location.

Other non-surgical methods of treating Morton’s neuroma include injectable cortisone and chemical sclerosis of the intermetatarsal nerve. Cortisone has been used successfully for years in treating Morton’s neuroma. Although the use of cortisone does not actually treat or change the entrapment of the intermetatarsal nerve, cortisone can decrease inflammation and swelling of the nerve, resulting in a decrease in pain. Care should be exercised when using cortisone injections noting that excessive cortisone injections can thin the plantar fat pad of the foot.

Sclerosis of the nerve (also called chemical neuro-ablation or chemical neurolysis) can be performed in the office using a number of different solutions, most commonly dilute (4%) alcohol. Multiple sclerosing injections are used to destroy the contents of the peripheral nerve. A series of injections are employed, each injection separated by a period of 7-10 days. The total number of injections may vary from 3 to 7. The success rates of injectable sclerosing solutions have been reported to be as high as 60-90%. Chemical neurolysis is also a great tool for failed neuroma surgeries where a stump neuroma has formed.

The intent of chemical neurolysis is to destroy the internal contents while preserving the external sheath of the nerve. This would be a bit like removing the copper wire in an electrical wire while preserving the plastic outer insulation or cover of the wire. The reason that this is important is due to the fact that peripheral nerve will regenerate over time. With the nerve sheath intact, regeneration of the nerve is possible in a controlled manner utilizing the existing sheath. By contrast, removal of the nerve by surgery results in the nerve regenerating and the formation of a mass of scar tissue called a stump neuroma. Knowing that peripheral nerve may regenerate also means that sclerosing injections may need to be repeated at some point in the future. The percentage of repeat sclerosing injections varies but is overall quite low.

Another new technique used to treat Morton’s neuroma is called cryogenic neuroablation. Cryo surgery is surgery that uses extremely cold instrumentation to selectively destroy tissue. Cryosurgery has been used commonly to destroy superficial skin lesions such as warts and moles.  The technique uses what is referred to as the Joule-Thompson effect. The Joule-Thompson effect occurs when a gas is passed through an area where it may expand. As the gas expands, it cools to approximately -70 degrees centigrade . In the case of cryogenic neuroablation, the expansion of the gas is controlled in a 5.5 mm probe that freezes and subsequently destroys the nerve tissue.

In the cryogenic ablation study carried out by Drs. Caporusso, Fallet and Savoy-Moore, thirty one neuromas were treated in 20 patients. All procedures were performed in an office setting. The procedure used a small amount of local anesthetic to numb the skin to allow the passage of a 12-gauge cannula through the skin. A nerve stimulator was passed through the cannula to locate the nerve. Once the position of the nerve was established, two three minute freeze sessions were utilized to destroy the nerve tissue. A sterile dressing was applied to the site and the patient was dismissed without the need for pain medication. The study cites a 65% success rate.

Dr. Morton’s original treatment plan as described in 1876 included changes in shoes, multiple injections of cortisone and if necessary, complete excision of the common intermetatarsal nerve. We’ve mentioned before that Morton’s neuroma is a nerve entrapment much like carpal tunnel. Now let’s see if we can apply Dr. Morton’s treatment plan to any other nerve entrapment such as carpal tunnel syndrome. Perhaps we’d splint the wrist, try some injectable cortisone, but completely excise the nerve? No way. But that’s what’s been done for the past 100 years for Morton’s Neuroma. Post-op complications were common and included thinning of the plantar fat pad and loss of sensation in the 3rd and 4th toes.

The introduction of Dr. Barrett’s EDIN procedure has revolutionized the treatment of Morton’s Neuroma and really represents the first unique contribution to treating this condition in over 100 years. The EDIN procedure stands for endoscopic decompression of the common intermetatarsal nerve. Interestingly enough, Steve describes first thinking about this procedure as he watched another surgeon perform an endoscopic carpal tunnel surgery. Steve recognized the problem to be the ligament and not the nerve. The EDIN procedure selectively releases the ligament and leaves the nerve intact.

The EDIN procedure provides us with a new alternative. In the past we knew that the traditional surgery used to treat Morton’s Neuroma, called a neurectomy, was destructive and carried with it a number of post-op complications. Therefore, we would tend to use excessive amounts of cortisone to avoid surgery. The EDIN procedure provides a new alternative using non-invasive endoscopic techniques that usually return patients to activities much sooner than the traditional surgery. And, what I find most helpful is the fact that it enables us to use less cortisone, thereby avoiding fat pad atrophy. The question remains; was the common complication of fat pad atrophy due to the neurectomy itself or did it result from the overuse of cortisone? The EDIN procedure shows none of the traditional post-op complications that were so commonly seen in the neurectomy, therefore we can assume that fat pad atrophy was in part due to overuse of cortisone.

The EDIN procedure has been used for at least ten years and has shown promising results. It can be technically challenging for some who are not familiar with endoscopic techniques. As with other surgical procedures there are pros, cons and possible complication that need to be discussed thoroughly with your physician prior to surgery. The following pictures show the technique used to perform an EDIN procedure. Image 1 shows pre-operative markings identifying the 3rd and 4th metatarsal heads. Image 2 shows placement of the cannula through an interdigital incision. The cannula is much like a small 4mm drinking straw with a slot cut in one side. The slot or open side of the cannula is placed adjacent to the intermetatarsal ligament. The cannula passes from between the toes to a second incision on the plantar aspect of the foot just proximal to the weight bearing surface. The endoscope and knife are used within the slotted cannula to identify and transect the intermetatarsal ligament. Image 3 show the use of a blunt probe without the cannula to verify a complete release of the intermetatarsal ligament. In the bottom of image 3, a metatarsal spreader can be seen. The spreader is used to separate the 3rd and 4th metatarsals subsequently putting pressure on the intermetatarsal ligament. The procedure takes about 20 minutes and is completed in a hospital or surgery center. Local anesthesia with sedation is used. Patients return to regular shoes in two days with just a band-aid on the incisions.

EDIN_procedure_for_Morton's_neuroma_image1 EDIN_procedure_for_Morton's_neuroma_image2 EDIN_procedure_for_Morton's_neuroma_image3 EDIN_procedure_for_Morton's_neuroma_image4

Traditional neurectomy, or removal of the nerve for the treatment of Morton’s neuroma, is used less often due to the success of sclerosing injections and the EDIN procedure. Neurectomy can be performed from a dorsal or plantar approach. The advantage of a dorsal approach is that patients are able to walk immediately following the surgery. The disadvantage of the dorsal approach is that it requires more dissections and possible tissue trauma. The plantar approach results in less tissue trauma but requires that patients are non-weight bearing on the surgery foot for 3 weeks post-op.  Traditional neurectomy for the treatment of Morton’s neuroma is performed on an out-patient basis at a surgery center or hospital using a local or general anesthetic.  The procedure is completed in less than 30 minutes.

from youtube: