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I. Multiple Sclerosis Overview” Introduction [S1]:
a. How common do you think MS is?
b. The National Institute of health and the CDC classifies MS as a rare disorder. There are about 350,000 –
450,000 people in the U.S. who have MS. The risk of having MS is about 1/800 people.
c. How do MS patients present? Who is a typical MS patient?
d. Caucasian females are the most common.
II. Patient Scenario [S2]
a. This is a typical case.
b. 26 year old Caucasian female
c. Acute onset visual loss in right eye- monocular vision loss.
d. Ophthalmology examination shows a Relative afferent pupillary defect- a Marcus-Dunn pupil on the right side.
e. VA: 20/70 OD, 20/20 OS- worsening of visual acuity on the right side.
f. Red desaturation OD- Color desaturation, which is fairly common.
g. She has pain with extraocular movement when you ask her to move her eyes.
h. She has a stinging pain behind her eye.
i. Central scotoma on confrontational VF test
j. She has Papillitis and some atrophy light changes on her frontoscopic exam.
k. What does she have?
i. She has optic neuritis. She has inflammation in her optic nerve that has caused her to have vision loss.
The most common diagnosis for a young woman with symptoms like this is MS.
l. The next thing you would do would be an MRI of the brain and the orbits.
i. In an orbit MRI we would look for an enhancement or active inflammation in the optic nerve, which you
would see if this episode is within the last 14-28 days.
ii. You would also do an MRI of the brain.
III. Patient Scenario [S3]
a. This is her MRI of the brain, which is normal.
b. This is called a flared image. It shows any changes in the white matter. This is normal.
c. If someone presents with optic neuritis and has a normal MRI of the brain, her likelihood of developing MS
would be low.
d. Based on our natural history studies she has about a 15 % chance that she will develop MS over 10 years.
There is an 85% chance that she does not have MS.
IV. Patient Scenario [S4]
a. What if her MRI showed this?
b. This person has a lot of these white spots on the MRI as opposed to the last person whose MRI was normal.
c. These lesions are fairly typical for someone with MS. If this lady with optic neuritis had this MRI, her chance of
developing MS would be about 85-90%.
d. When you have someone that presents with monocular vision loss where you suspect that they have optic
neuritis, the key test for that person from a neurologic standpoint is an MRI of the brain. If the MRI is normal that
person’s likelihood of developing MS is only about 15% over 10 years. If they have an abnormal MRI, their
chance of developing MS is about 85-90% over the next 2-3 years.
e. One of the key points that you should take home is that MRI has been very helpful in establishing a diagnosis of
MS and for us to tell a patient whether they should expect more symptoms and problems in the future or not.
V. Patient scenario [S5]
a. Treatment- We would treat this person with steroids. We will talk more about this when we talk about prognosis
and treatment in a minute.
b. Prognosis
c. Follow-up
d. This would be a typical presentation for someone who develops MS.
VI. Disorders of White Matter [S6]
a. MS is the prototypical white matter disease of the brain. There are two types of white matter diseases we see in
neurology.
b. Dysmyelinating disease or dysmyelinating disorders
i. Where the myelin is never formed normally. Usually patients have a genetic abnormality that leads to
development of abnormal myelin and leads to disorders like leukodystrophies. These are disorders that
generally present as a child- in infancy or early childhood. Sometimes in teenage years. Very rarely as
adults. These kids are usually seen by pediatric neurologists.
c. Demyelinating disease/disorders
i. These are much more common in adults. These are disorders where a person would have normal myelin
development initially. They would have normal growth, moderate cognitive millstones, but later on in their
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life something damages their myelin and results in demyleination or loss of myelin or damage to myelin.
These are the patients that are commonly seen in his practice.
d. MS is the most common demyelinating disorder. This is a disorder where there is damage to the myelin once it
has formed normally. It affects the site matter of CNS- brain and spinal cord only.
e. What produces myelin in the CNS? Which cells? Oligodendrocytes.
f. What do Schwann cells do? Produce myelin in the PNS.
g. Peripheral myelin is produced by Schwann cells. That is what is affected in neuropathies.
h. Central myelin is produced by oligodendrocytes. They are the cells that get affected in MS so we get myelin
damage only in the CNS.
i. Patients with neuropathies have numbness distally, symmetrically.
j. Patients with MS can have numbness.
k. The site of the lesion is different in those two diseases. MS is a disease of the CNS only. Patients typically do
not have peripheral neuropathy.
VII. Multiple Sclerosis [S7]
a. The hallmark of MS is there is dissemination of neurologic problems separated in time and space.
b. Someone who presents with a single event like the first person I presented with optic neuritis, you cannot say
that person has MS, even with an abnormal MRI. That person has a single event. To call it MS you have to
prove that person has dissemination in time and space, thus they have neurologic involvement in different areas
of the brain or spinal cord that are separated in time, typically separated by 30 days.
c. Somebody who has optic neuritis and then 3 months later they develop numbness and weakness on one side of
their body. That person has MS because now they have two different events separated by 30 days.
d. If someone has only a single event we call it clinically isolated syndrome. We don’t’ call it MS because by
definition we have to have multiple events separated in time and space.
e. That lady with optic neuritis, I would do an MRI. If the MRI was abnormal I would tell her that she would have a
very high likelihood- about a 90% likelihood that she would develop MS and that she would have more problems
in the future, but I could not call it MS at this time based on our current criteria.
VIII. Challenges for the healthcare provider [S8]
a. The problem with MS is that there is a challenge in diagnosis.
b. Difficult diagnosis
c. No single specific test- including MRI that tells us that a person does or does not have MS. The white spots that
I mentioned earlier- you can see those in lupus. You can see them in B12 deficiency. You can see them in
Lyme disease. You can see them in a whole lot of other disorders, so you have to interpret the MRI in the
clinical context. You cannot use MRI in isolation to diagnose MS.
d. Similarly spinal fluid abnormalities: you can see abnormalities similar to MS in other disorders, and you can
have MS patients with normal brain MRI, normal spinal fluid, and so forth.
e. In the absence of a single diagnostic test, what you are left with is trying to make a clinical judgment based on
all the clinical data available.
f. No two cases of MS are alike. There are some common symptoms that patients with MS have but they occur
in different combinations. A person may present with complete visual loss or they may present with just visual
blurring on that side. They may present with numbness in the hand, numbness in the leg, weakness in one part
of the body or another, and double vision. They can present with a variety of different neurologic symptoms.
g. No proven cause
h. No known cure
i. MS is unpredictable- although most of the patients with MS will become disabled; the rate of progression of
disability (how quickly they become disabled) is very different in different patients.
j. Partially effect treatments- although they help the patients, they are not perfect.
k. All of these problems are a problem in diagnosing and treating MS.
IX. Epidemiology of Multiple Sclerosis [S9]
a. Age: Most of the patients who develop MS are young. 20-40 yrs (mean 30 yrs). 80-85% of people with MS will
present in this age. 10-15% of people present after the age of 40, and 5% of patients present under the age of
20. In his practice the youngest person that he has diagnosed with MS was just under 40. The oldest diagnosed
for the first time was 67 years old. You can have people at all age groups, but most people are going to be
between 20-40 with the mean age around 30.
b. F:M ratio: 1.5-2.0 : 1 - It is more common in females.
c. Race:
W > B > Other racial groups. More common in Caucasians, especially people of Scandinavian or
European descent. All ethnic groups can get MS.
d. Incidence:
Worldwide
2.5 million
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US
365,000 – 400,000. There are 4,000-5,000 people with MS in Alabama.Clusters/”Epidemics”:
Faroe Islands, Iceland
e. Effect of migration:
Exposure at < 15 yrs of age is important
X. Epidemiology of Multiple Sclerosis [S10]
a. Geographical association: MS seems to occur more commonly the farther you get away from the equator. If you
get toward the northern or southern latitudes like Southern Australia, the risk of MS seems to be high.
b. This is a map of MS. The white areas are where we don’t have any data. The black areas are where there is
the highest incidence of M.S.
c. Why do you think these black areas have higher incidences of MS?
d. Student Answer: Different diagnostic procedures.
e. Response: Probably not.
f. There is thought to be a genetic correlation.
g. One of the hypotheses is that it is a genetic influence. What I mean by that is that people who are of northern
and Scandinavian descent were more likely to immigrate to the northern US or Canada, which has one of the
highest incidence of MS in the world. These same people were more likely to migrate to southern Australia.
There is probably a genetic influence that the Scandinavians and northern Europeans carried with them when
they immigrated.
h. The second hypothesis that we have is that there is probably a viral or environmental influence that is more
common in temperate climates as opposed to equatorial climates. There may be a virus that is more prevalent
in these regions that may trigger MS in patients who are genetically predisposed. That is the current hypothesis
for explaining why MS is variable in different geographical locations.
XI. Epidemiology of Multiple Sclerosis [S11]
a. MS is a lifelong disease. People with MS have nearly the same life expectancy as their age-matched control.
MS is not a fatal disease. People do not die from MS. They become disabled from MS. If left untreated, 30% of
MS patients will become wheel chair bound or bed bound.
b. 90% of people will develop a significant disability that will affect their day-to-day activities.
c. It is a disabling disease.
d. Example: 30-year-old or a 26-year-old who develops a neurologic disability. This is not only going to affect their
family life themselves but also professionally and productivity and cost.
e. In 1998 the MS society did a survey, and they estimated that MS is a very expensive disease if left untreated
because there is a lot of cost directly and indirectly to the community of not treating.
XII. Pathophysiology of Multiple Sclerosis [S12]
a. Here is what we think happens in MS.
b. Genetic Factors: We think that it is a genetic disease only partially. It is not a genetic disease where you can
pass a gene from the parent to the child and the child gets MS.
c. It’s a polygenic disease. A number of genes have to come together and predispose an individual to developing
MS. The genes only increase the likelihood of developing MS but don’t cause MS.
d. That person has to be exposed to something in the environment to then later on develop MS.
e. It’s a combination of both genetics and environmental factors.
f. Most people think it’s a viral infection although no one has ever found a virus that causes MS.
g. The combination of these two would lead to developing MS.
XIII. Pathophysiology of Multiple Sclerosis [S13]
a. This shows that you have a genetic influence, probably environmental and viral influence that leads to an
abnormal immunologic response which causes MS
b. MS is believed to be the result of an abnormal immunologic response to an infectious agent and/or unknown
environmental factors in people who have a
genetic predisposition to MS.
XIV.
Molecular Mimicry video [S14]
a. Skipped
XV. Progress in determining the causes and treatment of multiple sclerosis [S15]
a. Skipped
XVI.
Activation of Immune System in MS [S16]
a. It’s easy to explain this with a video more than what I can explain, so I’m going to show this video to you all.
b. He showed a movie at this point. I believe we are supposed to get the links to these clips.
c. When the immune system malfunctions in MS, the result is an attack on the body’s own myelin, including its
myelin-producing cells- the oligodendrocytes.
d. This attack is thought to be due to a complex interaction among several components of the immune system
including macrophages, cytotoxic T cells, B cells, and various cytokines such as Gamma Interferon and
interlukins.
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e. The immune response is initiated outside of the CNS when a cell antigen such as a myelin-type protein, possibly
a virus, is phagocytized by a macrophage and subsequently presented to an inducer T cell.
f. The inducer T cell then becomes activated and releases a number of cytokines into the blood including
interferons and interlukins. These cytokines act on other immune system cells such as B cells and other T cells
to further augment the immune response.
g. Cytokines such as gamma interferon cause the endothelial cells lining the blood vessels to express certain
adhesion molecules. Once activated T cells bind these adhesion molecules and essentially walk thorough the
blood-brain barrier into the CNS.
h. The first step in what we believe in MS is a genetically predisposed individual gets exposed to a virus, and the
virus activates the lymphocyte which in turn produces a lot of different chemokines and cytokines that stimulate
other T cells and also these make the cell go through the blood-brain-barrier and into the CNS. That’s where the
rest of the process starts.
XVII. Inflammation and the CNS in MS [S17]
a. He showed a movie.
b. In the CNS activated T cells are stimulated to release pro-inflammatory cytokines locally and the process
repeats itself. Simultaneously other immune system cells including B cells and macrophages also enter the CNS
through the blood-brain barrier, which further enhances the local immune response against myelin. B cells
produce antibodies that directly attack myelin and oligodendrocytes while macrophages function within the CNS
to phagocytize myelin.
c. The symptoms seen in the acute attack of MS are thought to be due to the problems of nerve conduction
caused by axonal demyelination and disruption. The inflammation and edema that can result from breaching the
blood-brain barrier are also thought to result in central nervous system damage.
d. Remission of symptoms occurs when the inflammation subsides. As time progresses, ion channels redistribute
along the axon.
XVIII. Axonal Damage and Lesion Formation in MS [S18]
a. In addition, oligodendrocytes proliferate and some remyelination of the axon occurs.
b. Damage to the axons themselves also occurs in MS. Once stripped of their myelin sheath, the exposed axons
are susceptible to further injury from cytokines, complement, and other enzymes, causing them to break and
disintegrate.
c. Throughout this time gliosis is occurring. Gliosis is the process by where astrocytes proliferate and fill in the
damaged areas, producing the characteristic scars of MS plaques.
d. It is thought that the residual deficits that patients experience in MS are due to accumulating axon damage that
is irreversible. The chronic active MS plaque shows a gradient of pathological changes. The center of the plaque
represents older events and is often characterized by many demyelinated axons surrounded by gliosis.
Travelling outward toward the border of the plaque, the number of macrophages increases and there is ongoing
demyleination and remyelination. However, in more chronic plaques, there is no evidence of either
demyelination or remyelination, and these plaques rarely consist of demyelinated axons surrounded by severe
gliosis with axonal degeneration Axonal transection is the consistent result of demyelination in the rings of
patients with MS. This is important because axonal injury can result in permanent neurologic dysfunction.
e. The frequency of trans-sectioned axons is related to the degree of inflammation within each lesion.
f. Those immune cells, lymphocytes, once they get in the brain, they produce cytokinds that recruit more cells.
They also recruit B cells that change into plasma cells and produce antibodies that stimulate complement.
g. Through all these processes, there are a number of things that happen: demyelination, which is damage to the
myelin; axonal loss; transection of the nerve fibers; there is also gliosis which is basically scarring.
h. All these processes are going on in the brain, which leads to the symptoms of MS and damage.
i. If it occurs in the optic nerve, it will cause optic neuritis.
XIX.
Multiple Sclerosis – Gross Pathology [S19]
a. This is what an MS plaque looks like. This is a ventricle section through the brain, and these dark areas in the
white matter, around the ventricle, are lesions of MS.
XX. MS Lesion [S20]
a. If you look at it pathologically under the microscope, what we see is all of these areas, blue dots that you see,
and you see that axonal density is less and there is lymphocytic infiltration.
XXI.
Multiple Sclerosis Pathology [S21]
a. This picture summarizes what happens in MS pathology. This is a blood vessel, and these are lymphocytes
around the blood vessel. There is pretty vascular lymphocytic infiltration. These immune cells are coming out
from the blood vessel into the brain. There is demyelination.
i. This is a nerve fiber with normal myelin.
ii. This is a nerve fiber where the myelin has been damaged.
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b. There is axonal transection. This was a nerve fiber that was connected like this. This is the distal end and this is
the proximal end toward the nerve cell. It was damaged as a result of Ms inflammation. Now it is trying to
reconnect here, but it never does.
c. It is lost and it is going to die forever.
d. All of these things are pathology that is seen in an MS patient to a varying degree.
XXII. Effect of Mild Demyelination [S22]
a. This is what happens with normal myelin. This is what happens normally. This is saltatory conduction, but if
there is damage to the myelin, if you lose myelin, then the action potential cannot pass through a demyelinated
segment.
XXIII. Effect of Severe Demyelination [S23]
a. If it happens in a more severe way where you loose myelin, there is an axonal block. The action potential will
come to this spot and stop. If there is an axonal block or slowness of the conduction velocity across a
demyelinated segment, those nerves will not function, and patients are going to have symptoms.
XXIV. Remyelinating Oligodendrocyte [S24]
a. This process also occurs in MS patients. There is also remyelination. Patients tend to recover as well.
b. At least initially, patients will lose their vision and then it will come back, or they’ll not be able to walk and then
they’ll start walking again with steroids.
c. Later on this becomes permanent as more and more of the brain and the spinal cord get damaged.
d. Initially recovery is partially because of remyelination.
e. This is an oligodendrocyte, this red dot here. It is sending out processes to various demyelinated axons to try to
recover. If you could find a way to restart this process it would be a very effective treatment strategy. We don’t
have anything that would do that as of yet.
XXV. Gray Matter Lesion Patterns [S25]
a. MS patients have lesions in the grey matter as well as the white matter
b. They tend to develop fatigue, cognitive problems, and memory loss due to the grey matter lesions
c. There is more understanding of the grey matter effects over the last five years
XXVI. Symptoms at Onset of MS [S26]
a. When a patient presents with MS, these are the common symptoms:
b. With their first episode of MS, these will be the symptoms:
i. The most common symptom is not optic neuritis, though usually people think it will be a young female who
loses vision
ii. The most common presentation is numbness, typically of the hand or foot that gradually ascends to the
torso
c. Optic neuritis and vision loss is the 2nd most common presentation
d. Poly-symptomatic onset, a combination of optic neuritis and numbness or balance problems at the same time, is
the third most common
e. These three constitute most patients’ symptoms when they first present
f. There can be other presentations too
g. These are at onset
XXVII. MS: Common Symptoms [S27]
a. If you ask a MS patient what bothers them the most, you will see there are a lot of problems that they have are
the initial symptoms.
b. Bladder and bowel problems, loss of control of these, is the most common problem they have
c. Fatigue (a sense of exhaustion; physical or mental) is very common
d. Spasticity, sexual dysfunction, pain, cognitive problems are all very common too
e. A lot of times, even as physicians, we don’t think of these problems as symptoms of MS. We think of someone
in a wheel chair, someone who can’t use their hands, or people with balance problems or vision loss
f. However, a lot of times patients develop disability because of cognitive problems, fatigue, bladder and bowel
difficulties
g. A lot of time in clinic is managing the symptoms of patients with muscle spasms and fatigue after the initial
diagnosis has been made.
XXVIII. Forms of MS [S28]
a. There are many different flavors of MS.
b. The most common is relapsing and remitting MS, which is where the patient comes in and has optic neuritis and
vision problems, they get better for 6 mo, then have numbness or weakness that stays for a few wks or months,
then they get better (have relapses/attacks and then get better and the pattern repeats over time)
c. If untreated, they will go on to have secondary progressive MS (30% of patients have this)
d. 90% of patients with relapsing MS go on to have secondary progressive disease if left untreated
e. In secondary progressive MS, the patient has less typical attacks of MS, but they have gradual disability
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f. They find that the general activities (walking, bathing, dressing, seeing) get more and more difficult over a period
of months (can’t walk as far, need their walker more, coordination and bladder problems worsen)
g. These are gradual progressions over weeks, months or years; not acutely like in relapsing MS
h. About 10% of patients have primary progressive MS; present without acute attack of MS
i. Difficult to diagnose because they start to have gradual difficulty: spasticity and weakness in legs, develop
difficulty walking (most commonly), balance gets worse
ii. Over about 7 years, many of them need help walking through a wheelchair, walker or cane
i. A small group of primary progressive MS patients present with optic neuritis, but it doesn’t onset quickly like it
usually does with acute neuropathy (no loss of vision overnight or in two hours); they lose their sight gradually
j. Have to follow them over time to realize they have vision loss due to MS
SQ: Inaudible but the gist of the question was, are there dental problems the MS patient will present with that we need
to look out for?
A: Not that he can think of. MS patients are more likely to develop osteoporosis and develop a degeneration of the
mandible and maxilla. These are not due to MS, but are secondary. We frequently have to remember to remind MS
patients to go manage their overall healthcare (mammograms, eye care, dental care, etc.) because they tend to focus
on their MS symptoms so much that they forget to take care of the rest of their health needs. He has patients that
come in thinking that they have trigeminal neuralgia because of pain in their face, but it is really an abscess in their
tooth.
XXIX. Spectrum of MS disease activity [S29]
a. This is a summary of what we’ve talked about
XXX. Laboratory and Imaging Studies [S30-32]
a. Once someone presents with symptoms of MS, we’ll do these studies:
b. MRI: most helpful in MS
c. See the white spots on the brain and the atrophy
d. See the black holes where the brain has been damaged enough to lose tissue
e. See lesions in the spinal cord (S31 shows lower part of brain and the spinal cord, a longitudinal section through
the neck, and see the white lesion on the cord)
f. These are common findings in MS
g. The next test that we do is visual evoked potentials
XXXI. Visual Evoked Potentials [S33]
a. If he thinks someone has optic neuritis or have already recovered, do this test to see if it is actually optic neuritis
b. Visual evoked potentials measure how long it takes for the signal that you see with your eyes to reach the
occipital cortex where the visual center is.
i. A person looks at a TV screen that has black and white checkerboard that changes (white become black
and black become white) 100 times per minute
ii. This creates a contrast that shifts which produces a signal in the retina that is conducted to the visual
cortex
iii. A normal person’s signal takes 100ms +/-5 from the time you see it until it reaches the brain
c. In a MS patient, this is delayed; if you have a difference of 10ms or more between the two eyes or the total time
is greater than 110ms, then you have an abnormality in optic nerve- HELPFUL TO KNOW
d. Virtually 100% of people with optic neuritis will have delay in P100 latency (P100 because positive and 100ms)
e. It helps us to know if someone has had optic neuritis before
XXXII. Common CSF Abnormalities [S34]
a. We also do a spinal tap and look for oligoclonal bands
b. This shows normal and someone with abnormal protein strands in their fluid
c. 95-97% of people with MS would have these bands in their fluid, so helpful test
XXXIII. Revised MacDonald Diagnostic Criteria [S35-38]
a. There are many ways to diagnose MS. This depends on what their MRI and spinal tap shows and how many
attacks they’ve had.
b. Because there is no single test, researchers came up with these different criteria to have confidence in
diagnosing MS.
c. There are 5 paradigms that can lead you to diagnosing definite MS
XXXIV. Clinical Stages in Relapsing MS [S39]
a. This is the life of a MS patient.
b. They start out with a few lesions on their MRI, then have their first attack
c. These are followed by more attacks and lesions
d. They gradually have more disability.
e. Their burden of disease (how many lesions and scars on their brain) increases over time
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f. They change from a pre-symptomatic stage to a secondary progressive stage over time
g. Their brain atrophies: brain volume becomes smaller in size
h. These are the stages an MS patient would go through- relapses, more MRI lesions, more disability, and worse
brain disease
SQ: Are lesions appearing and disappearing?
A: No- these are new lesions. They are adding them. It’s like a scar, once a person has a lesion from MS, they
have them forever. They don’t go away. The burden of disease of the volume of brain affected by MS increases
by 8-10% per year on average. It keeps increasing over time.
XXXV. Multiple Sclerosis Treatment [S40]
a. There are different ways to treat MS.
b. Treatment of Relapse (“Exacerbation”)- they have an acute attack; we treat that specifically, then put them on
treatment to prevent disability and more relapses (treatment of the disease itself)
c. Treatment of Underlying Disease
d. Treatment of Symptoms- Manage bladder problems, cognitive problems, pains, spasms, etc.
e. Psychosocial Support- Must provide a lot of counseling to these patients to help them accept this disease. We
wouldn’t want to think about having to go on disability within ten years while we are in our twenties. You counsel
the patient about the stages, treatments, etc. to educate and work with them to help them accept the disease
and go on with treatment
f. Patient Education- Very important part of management, especially in MS because dealing with young adults
XXXVI. Acute Relapse [S41]
a. How do we treat relapses?
XXXVII. Treatment of an Acute Relapse [S42]
a. The main treatment is steroids. No other treatment has shown effective after an acute attack of MS.
b. When someone presents with numbness, weakness, they can’t walk, they are seeing double, they have
vertigo/dizziness-give steroids. After a few weeks of steroid treatment they are pretty much back to the way they
were before; symptoms recover quickly after being treated with steroids
c. Therapeutic Plasma Exchange or Plasmophoresis is used for steroid unresponsive and severe relapses only
XXXVIII.
Relapsing MS [S43]
XXXIX. Treatment for Relapsing MS [S44]
a. After you’ve diagnosed and had initial attack treated, use different agents
b. In 1993, the first treatment for MS was made. Since then we have had 6 treatments approved for MS.
c. Interferon Agents
•IFN -1b (Betaseron)
•IFN -1a intramuscular (Avonex)
•IFN -1a subcutaneous (Rebif)
d. Non-Interferon Agents
•Synthetic Polymer: Glatiramer acetate (Copaxone)- approved in 1997
•Selective Adhesion Molecule (SAM) Inhibitor: Natilzumab (Tysabri)- approved in 2007
e. These slow down the disease activity so fewer relapses and less disability; can’t prevent every symptom
XL. Effect of Immune Modulatory Therapy [S45]
XLI.
SP MS [S46]
a. Usually a late stage.
XLII.
Treatment for SP MS [S47]
a. Interferon Agents
•IFN -1b (Betaseron)*- shown effective in European study
b. Non-Interferon Agents
•Anthracenedione Derivative: Mitoxantrone (Novantrone)**- chemotherapy drug; shown effective
c. These two are the mainstay of therapy for progressive MS
XLIII. Goals of Treatment of MS [S48]
a. Reduction in Relapse rate, people would have fewer attacks
b. Less disability overtime
c. MRI – less lesions
d. These are the positives of therapy, but there are some negatives too
e. Negatives include the fact that there are no pills, they are all injections
f. Betaseron is given every other day
g. Avonex- once a week in the muscle
h. Rebif- 3x per week
i. Copaxone- daily injection
j. Tysabri and mitoxantrone are IV infusions
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Scribe: Sheena Harper/Patricia Fulmer
Thursday, January 22, 2009
Proof: Sally Hamissou
Dr. Bashir
Neuroscience
Page 8 of 8
k. Patients have to change their lifestyle so they can give themselves injections
l. Oral form treatments are being tested; so far, none work
XLIV. PP MS [S49]
a. 10% of people with MS have this kind. No attacks, gradually worsen over time
XLV. Treatment for PP MS [S50]
a. Currently no treatments proven to slow or stop progression of disease, not even the ones that work for the other
two kinds
b. With these people you can only manage: try to maximize their function and improve quality of life
c. Very frustrating to manage because no treatments have had impact
XLVI. MS Symptom and Side Effect Management [S51]
a. Symptoms like spasticity, bladder problems, fatigue, depression have a number of treatment options available
b. Can’t treat for every single symptom they have because that would be too many drugs: only treat the small
number that are most disabling the patient
c. You can change which symptoms you’re managing depending on which symptoms that patient is struggling with
most at the time
d. Use a lot of different drugs to manage patient over time
XLVII. Other Demyelinating Diseases [S52]
a. There are a number of other demyelinating diseases in addition to MS
b. These are:
i. Acute Disseminated Encephalomyelitis- see ~1 case every other month
ii. Devic’s Diseases (Neuromyelitis Optica, NMO)- see ~1 to 2 cases per month
iii. Balo’s Concentric Sclerosis- see maybe 1 to 2 cases a year
iv. Marburg Variant- see maybe 1 to 2 cases a year
c. The bad thing is these diseases are much more severe than MS. People develop disability and could die from
these.
d. The good thing is that they are very rare.
XLVIII. Questions? [S53]
[end 45 min]
**He says he has a short paragraph summing up the videos