What is Spinal MS?

Maybe you have heard the term “Spinal MS.” What is that? I thought MS could be relapsing, primary progressive, secondary progressive, or “benign.”

The lesions caused by multiple sclerosis can occur anywhere within the central nervous system, which includes the brain, the spinal cord, and the optic nerves. Approximately 55-75 percent of patients with MS will have spinal cord lesions at some time during the course of their disease. If a patient does have lesions in the spinal cord, he/she may be said to have Spinal MS.

A smaller number of MS patients, approximately 20 percent, may have only spinal lesions and not brain lesions. I am an example of one of those 20 percent of MS patients who only have spinal lesions.

Symptoms of Spinal MS

Spinal MS occurs more commonly with lesions in the cervical spine (the neck area) in approximately 67 percent of cases. Lesions in this area often affect the corticospinal tract. Neurological signs which indicate lesions in the corticospinal tract include the Babinski Sign and the Hoffmann Sign. Additional indicators of lesions in the upper spine include the l’Hermittes phenomenon and the Romberg Sign. At one time or another, I have shown each of these signs of neurological involvement/interference due to MS lesions.

Although the location of lesions do not always closely correlate to areas of clinical disability, there are cause/effect patterns which do emerge. Patients with spinal cord lesions are more likely to develop bladder dysfunction (e.g., urinary urgency or hesitancy, partial retention of urine, mild urinary incontinence), bowel dysfunction (e.g., constipation or urgency), and sexual dysfunction (e.g., erectile dysfunction or impotence in men, genital anesthesia or numbness in women, pain with intercourse for either sex). Complete loss of bladder and bowel control may be lost in more advanced cases of MS.


Spinal cord lesions can also lead to sensory and motor deficits, including dysesthesias, spasticity, limb weakness, ataxia or other gait disturbances.

Read this post in its entirety:

What is Spinal MS?

Marcus Gunn Syndrome and Multiple Sclerosis

One test which my neurologist, ophthalmologist, and primary care doctor each conduct during every office visit is the “swinging flashlight test.” You know the one. The doctor asks you to look ahead then shines a penlight first toward one eye, then the other, alternating quickly to observe your pupils’ response to light.

I strangely enjoy this test because I know that my pupils will show something unique. Something which proves that I have damage to my optic nerve. My pupils show a Relative Afferent Pupillary Defect (RAPD) or Marcus Gunn Sign.

What does the doctor look for during the “swinging light test”?

The pupils (the black centers of the eyes which dilate or constrict in response to light) are inspected for size, equality, and regularity. Did you know that the pupils will constrict or dilate when you look at objects far or near? They do, which is kinda cool.

More importantly, each pupil should constrict quickly and equally during exposure to direct light and to light directed at the other pupil (the consensual light reflex). Using the swinging light test, the doctor can test and observe the pupillary response to consensual light in order to determine if there is a defect present.

Normally, the pupil constriction does not change as the light is swung from eye to eye. When the light is moved quickly from eye to eye, both pupils should hold their degree of constriction.

What is a Relative Afferent Pupillary Defect?

The Afferent Pupillary Defect (APD) or Relative Afferent Pupillary Defect (RAPD) is an abnormal and unequal response in the pupils of the eyes when exposed to light. It basically demonstrates that one optic nerve transmits a different message to the brain than the other one. Testing for RAPD is a good way to implicate or rule out optic nerve damage such as is caused by optic neuritis.


My temporarily blinding case of optic neuritis in 2000 left my right eye impaired. It doesn’t register light in the same way as my left eye as the optic nerve has permanent damage. When the doctor shines the light in my left eye (the “good” eye), both pupils will constrict. This is normal. When the doctor quickly moves the light to my right eye (the “bad” eye), my pupils begin to dilate since the brain thinks that less light is coming in. This shows that there is damage to the corresponding optic nerve.

Read this post in its entirety:

MS Signs and Symptoms: What is Marcus Gunn Syndrome?

Nystagmus and Multiple Sclerosis

Nystagmus is a condition that causes the eyes to make quick, repetitive, uncontrolled movements — from side to side, up and down, or in a circular pattern — making the eyes appear to bounce around. The jerky motion may be triggered by optical stimuli or physical motion, or may occur at rest.

Nystagmus can be mild, occurring only when a person looks to the side, or it may be severe enough to impair vision. Nystagmus often makes it difficult to focus steadily on a fixed object.

What causes nystagmus?

Nystagmus can be an inherited condition, showing up in early childhood, or it can develop later in life due to an accident or illness. Nystagmus is often a symptom of an underlying medical problem, such as stroke, multiple sclerosis, or head trauma. Other causes of nystagmus include severe nearsightedness, albinism, inflammation of the inner ear, central nervous system diseases, and medication side-effects. Sometimes the cause may be unknown.


In persons with multiple sclerosis, lesions in the brainstem and cerebellum may interfere with the nerve signals that affect motion of the eyes causing nystagmus. According to the MS Foundation, approximately 35 percent of individuals with multiple sclerosis may develop nystagmus. Abnormal gaze-holding mechanisms, vestibular imbalance, and impaired fixation are the most common causes of nystagmus in multiple sclerosis.

Read this post in its entirety:

MS Signs and Symptoms: What is Nystagmus?

Why Does the Neurologist Tap My Finger?

The neurologist is looking to see if there is a finger flexor response.  The finger flexor response is demonstrated by a sudden flexing of the thumb and/or index finger.  There are two ways to cause this response:

• The doctor snaps or flicks the nail of the middle or 4th finger.  A positive finger flexor response elicited in this manner is known as the Hoffmann reflex or sign.
  
• The doctor holds the middle finger while partially flexing it between his/her finger and thumb, then taps or flicks the underside of that finger.  A positive finger flexor response elicited in this manner is known as the Trömner sign.
  

What causes the thumb to flex?

The finger flexor response (Hoffmann relex or Trömner sign) is somewhat similar to the Babinski sign in that it is suggestive of a lesion or impingement along the corticospinal tract.

What is the corticospinal tract?

Very long nerve axons which originate in the part of the brain called the cerebral cortex travel through the brainstem, cross over at the top of the cervical spine and travel down each side of the spinal cord. This path is the corticospinal tract which is sometimes called the pyramidal tract since the area where the crossover of nerves occurs has a pyramid-like shape.

Corticospinal tract neurons are referred to as “upper motor neurons” but they do not control muscles directly. Neurons in the ventral horn that directly innervate (or stimulate) muscle are called lower motor neurons.  It is damage in lower motor neurons which causes atrophy of muscle, while damage in upper motor neurons does not.

How do the Hoffmann or Trömner signs differ from the Babinski sign?

Each of these signs indicate damage in the corticospinal tract. The Babinski sign indicates damage anywhere along the corticospinal tract. However, the Hoffman and Trömner signs are a bit more specific in that they indicate a lesion or damage above the C5 or C6 level of the cervical spine.

Read this post in its entirety:

MS Signs and Symptoms: What is the Hoffmann Reflex?

Is CIS the same as MS?

When someone experiences a single demyelinating or inflammatory attack of the central nervous system that causes neurological symptoms resembling MS, it is called clinically isolated syndrome, or CIS. Here are some common questions about CIS and how it is distinguished from other forms of MS.

Is CIS the same as MS?

According to updated recommendations redefining the phenotypes of MS made in 2014, CIS is considered an official form of MS. However, not everybody who experiences an episode of CIS will go on to develop full-blown multiple sclerosis.

How does CIS resemble other forms of MS?

An episode of CIS includes neurological symptoms that last for 24 hours or longer and are caused by inflammation or demyelination within the central nervous system (CNS). Myelin is the fatty substance that surrounds and protects nerves. Myelin helps to speed messages along nerves, and a loss of myelin serves to slow down the messages or keep them from getting through in the first place. A place where inflammation has attacked the myelin is called a lesion. The effects of demyelination are the same for each form of MS.

An attack of CIS can be monofocal — involving a single symptom related to a single lesion — or multifocal — involving more than one symptom caused by lesions in different locations in the CNS. The CNS includes the brain, spinal cord, and optic nerves. An episode of CIS is often followed by complete or partial recovery.

How is CIS diagnosed?

Similar to other diseases of the central nervous system, diagnosis of CIS may include laboratory tests to eliminate other potential causes of symptoms, a complete neurological exam to access function of the nerves, a thorough medical history, and magnetic resonance imaging (MRI) to look for evidence of inflammation or demyelination within the CNS. Depending upon symptoms, the recommended MRI given at this stage of diagnosis may only include the brain and not the spinal cord.

Read this post in its entirety:

What Is Clinically Isolated Syndrome?

The Basics of Primary Progressive MS

Not all forms of MS are the same. The majority of patients who develop MS begin with a relapsing form of the disease that features acute neurological attacks and a waxing and waning of symptoms.

Approximately 10 to 15 percent of patients who develop MS have a progressive form of the disease from the beginning that features steady worsening of neurological function with occasional plateaus or minor improvements. A number of patients with relapsing-remitting MS (RRMS) go on to develop the secondary progressive MS (SPMS) form of the disease.

Primary progressive multiple sclerosis (PPMS) can be more challenging to diagnose and is definitely harder to treat than relapsing MS. Since PPMS doesn’t feature distinct clinical attacks like RRMS, the criteria for diagnosis is different. According to the National MS Society, the criteria for diagnosis of PPMS are:

1. One year of disease progression (worsening of neurological function without remission), AND
   
2. Two of the following:
   

• A type of lesion in the brain that is recognized by experts as being typical of MS
• Two or more lesions of a similar type in the spinal cord
• Evidence in the spinal fluid of oligoclonal band or an elevated IgG index, both of which are indicative of immune system activity in the central nervous system   Fulfilling these diagnostic criteria may take years longer for PPMS than the equivalent does for RRMS.

Treatment for PPMS is limited.

Read this post in its entirety:
What is Primary Progressive Multiple Sclerosis?

What is optic neuritis?

Optic neuritis (ON) is an inflammation of the optic nerve, a bundle of fibers that transmits visual information from your eye to your brain. Symptoms of ON are varied, often including pain behind the eye and different degrees of vision loss. People with ON may experience blurry vision, blind spots, a graying out of vision, or dull colors. ON can, but does not always, result in temporary blindness and usually affects only one eye at a time. ON may be accompanied by flashes of light or new floaters which should be reported to your eye doctor and/or neurologist.

What causes optic neuritis?

Common causes of optic neuritis include demyelinating diseases, such as multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD, formerly known as neuromyelitis optica or Devic’s disease). In MS and NMOSD, the immune system attacks the myelin surrounding nerve fibers of the brain, optic nerves, or spinal cord resulting in inflammation and/or lesions that disrupt nerve signals to and from the brain. If NMOSD is suspected, a blood test can help distinguish it from MS and facilitate diagnosis.

Other causes of optic neuritis may include bacterial or viral infections (e.g., Lyme disease, cat-scratch fever, syphilis, measles, mumps, herpes), other autoimmune diseases (e.g., sarcoidosis, lupus), or drug side-effects (e.g., quinine, some antibiotics), according to the Mayo Clinic.

When I had the blinding case of optic neuritis in 2000, the results of my MRI showed inflammation of the optic nerve but no lesions.

I was not diagnosed with “post-infectious optic neuritis.” I had had a severe cold during the prior weeks. The MRI helped to eliminate the other potential diagnosis suggested, which was brain tumor. Fortunately, I did not have a brain tumor.

Read this post in its entirety:
MS Signs & Symptoms: Optic Neuritis

Use of Spinal Tap in MS Diagnosis

What is cerebrospinal fluid?

The central nervous system (CNS) is bathed in a clear, colorless liquid, called cerebrospinal fluid (CSF), that cushions and protects the brain and spinal cord. CSF is produced in the ventricles and helps to transfer waste products from the brain to the vascular system. It can also deliver nutrients and hormones to the brain. CSF is composed of cells, water, proteins, sugars, and other vital substances. Examining the fluid can help doctors to identify diseases affecting the central nervous system, including MS.

How is CSF collected?

Cerebrospinal fluid is obtained through a needle that is inserted into the spine during a procedure called lumbar puncture or spinal tap. For this procedure, the patient will usually lay on their side with their back arched (chin and knees tucked toward the chest). An area of skin on the lower back is cleaned before the procedure.

After the area is anesthetized (numbed), a thin and hollow needle is carefully inserted between two lumbar bones into the spinal canal, the space where the CSF circulates.

You may feel slight pressure as the needle is inserted. It’s very important to stay perfectly still during the procedure.

Read this post in its entirety:
Do I Need A Spinal Tap To Diagnose MS?

Evoked Potential Testing in MS

Multiple sclerosis (MS) is a complex demyelinating disease of the central nervous system for which there is no single diagnostic test. Common tools used to diagnose MS include the neurological exam, complete medical history, magnetic resonance imaging (MRI), and evoked potential (EP) studies.

What are evoked potentials?

As the brain “talks” to various parts of the body, messages are sent as electrical signals that travel along nerves. Demyelination and neurodegeneration caused by MS can disrupt these electrical signals. Evoked potential studies, also called evoked potentials (EPs), measure signals that travel through specific sensory nerve pathways in response to external stimuli. Those electrical signals are measured through sensors placed on the skin in combination with sophisticated computer programs.

Read this post in its entirety:
Evoked Potential Tests: How Are They Used In MS?

The Process of Being Diagnosed with Multiple Sclerosis

Being diagnosed with multiple sclerosis (MS) is a multi-step process that can take anywhere from days to years. Unfortunately, MS is not a condition where you walk into your primary care doctor’s office because of unusual symptoms, and you walk out of the office with a definitive diagnosis. Reporting your symptoms to your doctor is only the first step.

Step one: Early symptoms and preliminary tests

The neurological exam is the first step in trying to solve th

e mystery as to whether MS might be the cause of your symptoms. The doctor will look for signs to indicate that something may not be functioning as expected within the central nervous system (CNS) that includes the brain, spinal cord, and optic nerves.

To help eliminate potential causes of symptoms, your doctor may order some preliminary blood tests to rule out conditions such as vitamin B12 deficiency, lupus, autoimmune disease, Lyme disease, syphilis, or HIV. If the results come back normal, your doctor may then order an MRI of the brain and/or spinal cord.


Read this post in its entirety:
How Long Does It Take To Be Diagnosed With MS?

Can a Brain Tumor Be Confused With MS?

Diagnosing multiple sclerosis is not as easy as undergoing an MRI scan and having a neurologist watch you walk; instead, it is a challenging process, and neurologists want to get it right. One thing that was considered even before I underwent MRI scans in 2000 for optic neuritis was the possibility of a brain tumor. It turned out not to be a tumor, but I wasn’t diagnosed with MS at the time, either. Over the years, several patients have reported similar “not a brain tumor” diagnoses when telling their MS stories.

Can a brain tumor be confused with MS?

An extremely rare form of multiple sclerosis, called tumefactive MS, involves brain lesions that look like tumors. These lesions are usually larger and more aggressive than normal MS lesions. Treatment usually begins with high-dose intravenous corticosteroids (e.g., Solumedrol) followed by disease-modifying therapies for MS and symptomatic treatments.

In a recent study, researchers investigated the unusual concurrence of MS and brain tumors. They point out, however, that it is difficult to determine whether brain tumors in MS are more common than in the general population. People with MS undergo more MRI scans than healthy individuals, thus the diagnosis of brain tumors in MS patients may appear to be more frequent (Platone et al. 2015). But not all cancer-related brain tumors appear large; they can also look like multi-focal enhancing white matter lesions which are the hallmark of MS.

Read this post in its entirety:
Lymphoma May Be Confused For Multiple Sclerosis

Misdiagnosis and Multiple Sclerosis

Diagnosing multiple sclerosis is not a simple process, and even experienced doctors make mistakes. Even with improved testing tools and more detailed diagnostic criteria, MS misdiagnosis remains an important problem in neurology, with significant consequences.

Misdiagnosis is too common in MS

Rates of MS misdiagnosis range from 6 percent to 35 percent, based on a number of studies published between 1985 and 2005. There are several possible diseases that a person misdiagnosed with MS might have instead. Two of the most common missed diagnoses in these studies were psychiatric disease (23-27 percent) and migraine (9-10 percent).

In a more recent study (Solomon 2012), 95.1 percent of neurologists surveyed (n=122) had evaluated a patient, previously diagnosed with MS by another provider, who they “strongly felt did NOT in fact have MS.” Within the preceding year 39.7 percent of respondents estimated that they had seen three to five such patients. More than one-third (34.4 percent) reported seeing six or more misdiagnosed patients in the last year, including 20 (17.2 percent) respondents who had seen 10 or more such patients.

Read this post in its entirety:
Problems with Misdiagnosis of MS: But I Have ALL the Symptoms of MS!!

Being In MS Limbo

The road to diagnosis for MS can be long and winding for many patients. I’m happy for patients who receive their official diagnosis within just a few doctors’ visits. Not happy that they have MS, but happy that they can jump right in and get on with things; attacking the beast with medication, therapy, and determination.

For those of us who are not immediately diagnosed with MS, the feelings involved with the ‘not knowing for sure’ can be frustrating. Especially disturbing is when you suspect that your doctors do not believe you or your symptoms. The worst part may be when there is some clinical evidence that ‘something’ is not quite right, maybe there are lesions in the brain and obvious neurological symptoms, but your tests do not meet the standard diagnostic criteria for an official MS diagnosis.

That’s when the waiting game begins.

I was one of those patients who didn’t receive an immediate diagnosis. In fact, it took more than five years from what was my first obvious and debilitating attack (blinding optic neuritis) to the relapse that prompted additional testing that led to a diagnosis.

Read this post in its entirety:
What Is It Like to NOT be Diagnosed with MS?

MS Lesions With Central Veins Lead to Faster Diagnosis

Researchers in Nottingham, UK, have been trying to find a quicker and more accurate way of identifying MS in patients with an unclear diagnosis. To do this they have focused on T2-weighted MRI scans that can show both hyperintense MS lesions and their central veins, which appear hypointense in contrast. Lesions with central veins are called perivenous lesions. In reading your MRI report, you might see reference to periventricular lesions. These are lesions located near cerebral ventricles (a series of interconnected, fluid-filled spaces in the core of the forebrain and brainstem) that are common in MS.

What the researchers have found is that the percentage of lesions that are perivenous can predict whether a patient has MS. Using an ultra-high-field 7T MRI machine for a 2013 study, Mistry et al found that patients for whom more than 40 percent of their lesions had central veins developed MS. Those who had fewer than 40 percent of perivenous lesions did not have MS. This was true for 100 percent of the 29 patients included in the study.

Read this post in its entirety:

New Way to Evaluate MRI Scans May Lead to Faster MS Diagnosis

Celebrity Actress Reveals MS

When former Soprano’s star, Jamie-Lynn Sigler, publicly revealed her 15-year MS diagnosis in this week’s People Magazine and on Good Morning America, the news spread through the MS community like wildfire. Reactions were quite positive but many people wondered why it took so long for her to openly discuss living with MS.

Jamie-Lynn is one of 2.3 million people worldwide who live with multiple sclerosis, a progressive disease of the central nervous system that damages the insulation around nerves and results in a variety of symptoms. Some symptoms may be “invisible” such as numbness, tingling, impaired vision or pain, while others may be more noticeable, such as impaired mobility, weakness, tremors, or cognitive difficulties.

At the age of 20, Jamie-Lynn experienced heaviness and tingling in her legs, symptoms that led to her MS diagnosis. "It was a shock. I didn't feel sick. My ideas of MS were limited. I thought it meant, 'Wheelchair.' I thought it meant your life was over," she told People Magazine. As a public figure with invisible symptoms, there was no obvious reason to reveal her diagnosis so Jamie-Lynn kept it a secret with the full support of her family and close friends.

Read this post in its entirety:

“No superhero roles for me,” says Actress Jamie-Lynn Sigler Who Lives With MS

Being In Limbo Can Be Frightening, No Matter The Diagnosis

I’ve recently been reminded what it feels like to not know exactly what’s going on. To be told, “We found something and want to do more testing. You are scheduled for a procedure next week...that’s a lot like going to the dentist.” To sit in a consultation room shortly after the doctor leaves, pull out your iPhone and google the words she used, and begin to process what you’ve just been told.

Reality check

Last week I went in for my annual mammogram following which I received the standard all-clear in the form of a check-box report. No abnormalities detected. But since my breasts are very dense and I’ve developed lumpy bumpy cysts in recent years, my nurse practitioner had also ordered ABUS (automated breast ultrasound) which is a newer technology that can detect abnormalities in dense breasts that are not seen on mammogram. Ironically, my breasts were too large for the machine to be effective so the traditional hand-held, manual testing was done instead.

Besides the cluster of cysts in the right breast, the ultrasound unexpectedly found two solid masses in my left breast which is what prompted the brief meeting with a radiologist to schedule a core needle breast biopsy in a week. The biopsy took place on Tuesday afternoon and I was told that the report from the pathology lab should be back in 3-4 business days, probably by Friday. Not too long of a wait.

Read this post in its entirety:
Being in Limbo Can Be Frightening

New ICD-10 RA Diagnosis Codes

How does ICD-10 affect rheumatology patients and their doctors?
Rheumatoid arthritis (RA) was previously represented by the ICD-9-CM code 714.0. Now RA and its many manifestations are represented by more than 300 individual codes that are grouped under two main categories: Rheumatoid arthritis with rheumatoid factor (ICD-10-CM code M05), and Other rheumatoid arthritis (ICD-10-CM code M06).

The increased number of codes allows for greater detail in documenting the specific manifestations of RA-related disease activity, such as identifying that the left shoulder joint is affected, or that a patient has rheumatoid lung involvement, or whether a patient tested positive for rheumatoid factor.

In my own case of RA, my 714.0 Rheumatoid Arthritis diagnosis has now been changed to “M06.09 Rheumatoid arthritis without rheumatoid factor of multiple sites.”

Examples of other ICD-10-CM codes related to RA disease manifestations:

M05.10 – Rheumatoid lung disease with rheumatoid arthritis of unspecified site
M05.352 – Rheumatoid heart disease with rheumatoid arthritis of left hip
M05.419 – Rheumatoid myopathy with rheumatoid arthritis of unspecified shoulder
M05.719 – Rheumatoid arthritis with rheumatoid factor of unspecified shoulder without organ or systems involvement
M06.071 – Rheumatoid arthritis without rheumatoid factor of right ankle and foot
M06.239 – Rheumatoid bursitis of unspecified wrist
M06.331 – Rheumatoid nodule of right wrist
M71.20 – Synovial cyst of popliteal space [Baker] of unspecified knee

I’m not sure what code would apply if you had seronegative negative RA with rheumatoid lung involvement as the code for rheumatoid lung disease with rheumatoid arthritis is M05.1 which falls under the classification of M05 which is Rheumatoid arthritis with rheumatoid factor.

With all of this in mind, no wonder my soon-to-be-retired rheumatologist said that if she had known exactly when all of this was coming, she might have retired a month sooner.

What do you think? Would having this greater amount of detail hiding in the numbers lead to improved quality of care?


Read this post in its entirety:
What's Your New RA Code?

Do You Celebrate Your MS-Anniversary?

So I woke up this morning, trying to remember the date. Then I had this itchy little question in the back of my mind, “What’s supposed to happen today?” After which I remembered…

Today is my MS-iversary!!

It was ten years ago on this date that my neurologist simply informed me that, “Now, we can prescribe one of the disease-modifying drugs.” He didn’t say, “You have MS.” He just told me that my follow-up MRI showed more lesions so I qualified to start treatment. Plain and simple. No big fanfare. I was just ready to get moving on things and to start beating back this beast that was taking away my ability to perform.

That appointment in October was somewhat anticlimactic, however. The month earlier I had attended my neurology clinic’s annual MS seminar at which I was introduced to the specialized MS nurse from the clinic (whom I had yet to meet in the office). She asked me, “Do you have MS?” and my response was, “I don’t know yet.” She replied with a kind hand on the shoulder that I would not have received the mailing for the seminar if it wasn’t very likely I have MS.

MS was not a surprise by the time I received the diagnosis. It was just a turning point that opened up new options for what we could do.

So when I think of the anniversary of my MS diagnosis, I almost laugh. Which event exactly do I want to celebrate? How do I want to put MS into perspective within my life’s journey?

If I look back 10 years to the actual diagnosis date and calculate based on adult years, I’ve lived with MS for just over 34% of my adult life, or not quite 20% of my entire life.

If I look back at the case of blinding optic neuritis, I’ve lived with MS symptoms for 32% of my entire life, or 52% of my adult life.

Or if I go back even further – to the time in graduate school when I was having visual disturbances and the opthalmologist at the university clinic ordered MRIs of my brain/optic nerves – I have lived with a suspected neurological condition for 86% of my adult life.

So how long have I had MS? The official answer would be 10 years.

My apologies to my MS for almost forgetting our anniversary. We’ve been on this road together for so long, and have become so comfortable with each other and our many idiosyncrasies, that I almost forgot.


Read this post in its entirety:
How Dare I Forget My MS-iversary?

Living with MS for 10-15 Years So Far

Fifteen years ago, I became blind. In under two days, I went from ‘something is just not right’ to ‘all I can see is solid gray.’ It was terribly frightening and I wasn’t sure what to expect for the future.

One thing I knew at that time was that I did not have multiple sclerosis because my brain was clear of ‘white spots’ or lesions. I also didn’t have a brain tumor. I could walk just fine, so I probably didn’t have neuromyelitis optica (NMO) either. This was before the blood test was available to look for NMO markers to make diagnosis easier, but I was to return to the neuro-opthalmologist if I had trouble.

It was a busy March concert season with performances and rehearsals scheduled on more days than not. My calendar was a mess of scribbled notes regarding where and when I had to be in specific locations for work. There was the Baltimore Opera, Fairfax Symphony, National Gallery of Art Orchestra, and other freelance gigs. All of that on top of the 30+ private music students I had at the time.

I was busy, to say the least, and didn’t have time to mess with physical weakness or logistical limitations.

Figuring out how to get around to where I needed to be took a little bit of time since I wasn’t really safe to drive long distances. I felt like I could manage driving the two miles it took to go from my apartment to the school where I taught and I arranged to carpool to rehearsals and performances.

The same day I reached complete blindness in the right eye, I was almost late to a rehearsal in Baltimore. I had been waiting in line for much too long to have blood drawn for testing to help determine what might be going on. I apologized to the contractor for my almost tardiness. In professional settings, if you are not 20-30 minutes early, you are late!

Did I explain what was going on? No. I kept quiet about my struggles except to my new carpool buddy and one fellow horn player. My colleagues and students were left in the dark about my new challenges. But looking back, I must have been a mess with steroid poof, dark eyes, fatigue, bumping into things, etc.

When I talked with my friend, the horn player, she told me that her mother has lived with MS for years. Bless her heart, my friend did not tell me anything which would have scared the living daylights out of me - although I wasn’t seeing half of daylight anyhow - when she could have. She spoke with the wisdom of someone who has loved someone with MS for many years. Thank you, Jennifer.

After my vision returned, I went on with life blissfully for several years. But when I began to feel numbness and tingling in my left hand and arm, and eventually lost use of the same, I knew that my luck had run out. I had not managed to escape the grips of multiple sclerosis afterall.

Ten years ago when I was once again referred for MRI scans, I knew what they would show. I knew that this time there would be ‘white spots’ or lesions. This time the answer would be clear. It was, but that didn't prevent me from needing a spinal tab and further MRI scans. All told, it still took another five months before the news became official - You have MS.

So now that I’ve been living with MS, officially, for ten years, I try to speak with the wisdom of my friend Jennifer. It’s good to share information and support with those who are facing diagnosis and an uncertain future. It’s also good to simply offer an empathic ear to listen to the fears and concerns of others.

Even those of us who have lived with this disease for many years still do not know what the future holds for us. Right now, my future looks good. I’ve found a treatment regimen which works and keeps me functioning at a high level. I will never be able to do many of the things I once did, but that’s okay. I’m doing many other things which I never dreamed of through advocacy and outreach.

Life is different than I had dreamed and was working towards 15 years ago. But I bet that is true for anyone, regardless of disease. Life is an evolving experience and we are here to discover a path and live it to its fullest.


Read this post in its entirety:

Anniversary of an Early Non-Diagnosis and Living a Fulfilling Life

Early Signs of RA

Fatigue. One of the most common symptoms of several autoimmune diseases is fatigue; RA is no exception. You may experience fatigue before any other symptoms become obvious. In a 2013 survey of more than 1,000 RA patients in the U.S. (conducted by HealthUnion), fatigue was exceeded only by hand/wrist pain as one of the most significant initial symptoms of RA in 56.3 percent and 69.6 percent of survey respondents, respectively.

Morning stiffness. People with RA often experience early morning stiffness that lasts for hours. Stiffness may also occur throughout the day following periods of stillness or inactivity. Osteoarthritis may also cause morning stiffness; however, it will usually last 30 minutes or less.

Joint swelling and tenderness. Mild inflammation which accompanies stiffness may cause joints to appear larger than normal. The inflammation and swelling may also make joints feel warm to the touch and appear red. However, joint swelling may be so subtle as to make it difficult to identify, especially in obese patients.

Joint pain. The pain of early RA frequently involves specific joints of the hands or feet, including the metacarpophalangeal joint (MCP) at the base of each finger, the proximal interphalangeal joint (PIP), or the metatarsophalangeal joint (MTP) at the base of each toe. Keep in mind, however, that early RA pain is not limited to the hands and feet; larger joints may be involved.

Decreased range of motion, numbness, or reduced grip strength. Inflammation can affect tendons and ligaments as well as synovium, restricting range of motion, fluidity of motion, or physical function. Inflamed tendons may put pressure on nerves leading to numbness or weakness. In the 2013 survey mentioned above, 39.9 percent of respondents included reduced grip strength as an early symptom of RA, while 32.7 percent noted general weakness.

Low-grade fever. Often accompanied by general malaise, and in the presence of other symptoms, a low-grade fever may be an early warning sign of RA or a flare-up. However, a temperature above 100°F (38°C) is more likely to signal some other illness or, possibly, an infection.

Abnormal laboratory results. Studies show that anti-cyclic citrullinated peptide (anti-CCP) antibodies may be detected in healthy individuals years before the clinical onset of RA. Most, but not all, people with RA test positive for rheumatoid factor (RF). Nonspecific inflammatory markers, such as erythrocyte sedimentation rate (ESR or sed rate) or C-reactive protein (CRP), are often elevated, but test within normal ranges in about 60 percent of patients with early RA. Additional abnormal blood tests may include high platelet count, low albumin, raised alkaline phosphatase (a liver enzyme), or normocytic-normochromic anemia.

Firm lumps of tissue located under the skin. Rheumatoid nodules tend to grow close to joints affected by RA, such as elbows or wrists. They may be as small as a pea or grow to the size of a walnut. Nodules can also form on vocal cords, or appear in the lungs, heart or other organs.

Extra-articular symptoms. Patients with early RA may develop vasculitis, inflammation of the blood vessels, or serositis, which involves inflammation of the tissue lining the lungs (pleura), heart (pericardium), or inner lining of the abdomen (peritoneum). Pleurisy (inflammation of the lungs) can cause chest pain when you breathe.

Read this post in its entirety:
What are Early Signs of Rheumatoid Arthritis?