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Multiple Sclerosis Multiple Sclerosis (MS) is an autoimmune disease, which means the body’s immune system attacks a part of itself. With MS, the immune system attacks the myelin sheath that covers nerves in the brain and spinal cord. The messages traveling along these damaged nerves may be slowed or blocked, resulting in a delayed response to external stimuli. Ultimately, damage to the myelin sheath may result in irreversible deterioration of the nerves themselves. This is what makes MS a potentially debilitating disease.

Incidence and Diagnosis MS is a relatively rare disease, affecting approximately 1 in 1,000 people1. Prevalence is currently estimated at 2.3 million people worldwide. Multiple Sclerosis is the most common chronic, disabling neurologic disease among young adults. It can occur at any age, but is most commonly diagnosed in people between the ages of 20 and 40, affecting women at least twice as often as men.1

Causes of MS Patients may have genetic predisposition to MS, but it is not an inherited disease. The

risk of multiple sclerosis is higher for persons who have a family history of the disease such as a parent or sibling. It’s interesting to note that an identical twin has about a 30% chance of developing MS if his or her twin has the disease.1 A slightly increased risk also occurs in patients who have thyroid disease, juvenile onset diabetes (type 1) and/or inflammatory bowel disease. MS appears to be triggered by some factor or factors in persons who are genetically susceptible. Potential triggers may be environmental or virologic. For example, a higher incidence of MS occurs in countries positioned farthest from the equator. Vitamin D may play a role, as research shows it positively benefits the immune system function. Some researchers are examining viral or bacterial exposure as a potential trigger. In addition, certain pathogens including measles, herpes virus-6 and Epstein-Barr virus are being investigated for their role in MS.

Immune System Role The immune system is a complex, interactive system with multiple parts and functions that are critical for

survival. With autoimmune diseases like MS, it is primarily the functions of protection and tolerance that can go awry. The normal immune system is designed to recognize and differentiate both invading antigens and the body’s own cells. Every cell in the body carries distinctive molecules that identify it as “self.” A molecule that is recognized as “non-self,” for example bacteria, pollen for some people, and human tissue (as in organ and bone marrow transplantation), is an antigen. Each antigen has its own distinctive markers. The greater the difference between the antigens and “self,” the stronger the immune response. The normal immune system allows for both innate and adaptive immune responses to antigens. It is the adaptive arm of the immune system that is most significant in autoimmune disease. When an antigen presents it is seen as foreign or “non-self,” the T-cells or T-lymphocytes attack and destroy it. T-cells are also the catalysts for B-cell, or antibody, production. Antibodies play an important role in the adaptive immune response in which B-cells form antibodies and establish a

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Inflammatory Process in MS In MS, antibodies have developed against the protective fatty covering of nerves of the central nervous system—the myelin sheath. During inflammation, the myelin gets stripped from the axons (demyelination). When the myelin sheath is damaged, the transmission of nerve impulses is slowed, stopped or can jump across into other demyelinated axons. The inflammation can also damage the underlying

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As the myelin around the nerves is damaged, the ability of the nerves to conduct electricity is lessened. Depending on which nerve fibers are affected, patients can experience problems ranging from weakness and clumsiness to numbness, burning or tickling sensations, visual disturbances, and even emotional and cognitive changes. Since the areas of damage are variable, the disease itself is unpredictable in terms of its clinical presentation. Patientspecific symptoms depend on the site of involvement and the degree of myelin or nerve damage.

The Four Forms of MS 1. Relapsing/remitting MS (RRMS) is the most common form, affecting approximately 85% of patients with MS.2 RRMS presents as a clearly defined bout of symptoms, followed by spontaneous remission during which all or most of the symptoms diminish or resolve. Eventually, however, full resolution of symptoms does not occur, resulting in residual disability that is additive over time.

2. Secondary Progressive MS (SPMS) follows on a course of RRMS and develops in about half of the patients with RRMS within ten years.2 Over time, distinct relapses and remissions become less apparent and the disease begins to worsen steadily. Occasional flare-ups, minor improvements, and even periods of stability may occur, but overall, the picture is one of accumulating disability. 3. Primary Progressive MS (PPMS) describes a course of MS that is characterized by a slow accumulation of disability without relapses. Approximately 10–20% of people diagnosed with MS have PPMS.2 It is the only form of MS to affect men and women equally and tends to be diagnosed after age 40.2 4. Progressive-relapsing MS (PRMS) is the rarest form, affecting an estimated 5% of patients with MS.2 Patients will experience clearly defined relapses but with steady disease progression. There are also two subtypes: Benign MS and Clinically Isolated Syndrome (CIS). Benign MS describes the

Increasing Disability

Normally, these antibodies are only directed at intruding antigens. However, when the body mistakes its own tissue as “the enemy,” or as “foreign,” antibodies form against “self.” In the case of MS, that “self” is the protective myelin sheath of the nerves in the brain and spinal cord. When the immune system can't distinguish between healthy body tissue and antigens, an immune response develops against the normal body tissues. This response is a hypersensitivity reaction similar to the response in allergies. In allergies, however, the immune system reacts to an external substance that it normally would ignore. With autoimmune disorders, the immune system reacts to normal body tissues. What initiates this autoimmune response remains unknown.

axonal membrane, further diminishing nerve transmission.

Increasing Disability

specific immunological memory, i.e. adapt, to that particular antigen. Whenever the body is re-exposed to a particular antigen, the B cells reactivate and again mark the antigen for destruction.

Time RR-MS with full recovery between relapses RR-MS with residual deficit between relapses

Time SP-MS with variable progression without relapses SP-MS with variable progression with relapses

Source: http://www.medicinenet.com/multiple_sclerosis_ms/article.htm

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presence of remission between relapses that is almost complete. Even 15 to 20 years after diagnosis, there is little if any accumulation of physical disability. In most cases of benign MS, symptoms mainly affect the senses of sight and/or touch. The proportion of people with MS considered to have a benign course is about 10% or less and decreases over time.2 A first occurrence of an MSlike neurologic symptom is termed a Clinically Isolated Syndrome (CIS). It is, for some people, the first indication of MS. However, only about 60% of people who experience CIS go on to develop MS. Several potential risk factors have been associated with a higher risk of developing MS including the presence of oligoclonal bands in their cerebrospinal fluid, two or more lesions on MRI brain scan and diagnosis of CIS at a young age.3,4 The results suggest that low levels of vitamin D also put people with CIS at a higher risk of developing MS; however, further studies are recommended to determine cause and effect related to Vitamin D.3,4

Symptoms of MS The clinical picture of MS is extremely variable in terms of symptoms, progression and treatment response. Symptoms vary from mild to severe; they may be ongoing or intermittent; tolerable for some patients, disabling for others; and treatable or non-treatable. Symptoms of MS often cycle, with signs of active disease

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alternating with a remission that can last for weeks, months or years. Typically, however, the disease gradually progresses and eventually produces varying degrees of disability. As a result of the irregular, intermittent or progressive impairment of sensory or motor function, patients may experience symptoms which typically resolve and for which, in the early stages, they do not seek medical attention. It is not uncommon for patients, at the time of diagnosis, to look back to when some of these symptoms were present and recognize those early symptoms as disease onset. Common and early symptoms include: yy Hyperesthesia (increased sensitivity to pain) yy Paresthesias (“pins and needles” or other tingling sensations) yy Visual disturbances »» Diplopia (double vision) »» Nystagmus (rapid, jerky rhythmic eye movement) yy Dysequilibrium, unsteadiness yy Muscular weakness or spasticity yy Tremors yy Compromised swallowing Less common and/or laterdeveloping symptoms include: yy Speech and swallowing problems yy Cognitive dysfunction yy Difficulty walking yy An inability to adequately empty the bladder yy Nausea, vomiting, abdominal fullness or bloating, diarrhea or constipation

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yy Low blood pressure with dizziness

yy Trouble maintaining an erection.

yy Mood swings, depression

Tools Used To Diagnose MS With intermittent symptoms and a lack of a single or specific test for MS, making a diagnosis is a challenge and often determined through a process of elimination over a long period of time. Newer guidelines, however, are designed to shorten the time to diagnosis—important since early treatment is critical. Three things need to be present in order to consider an MS diagnosis: 1. Evidence of two demyelinating events with damage in at least two separate areas of the CNS (including the optic nerve) 2. Evidence that the damage occurred at least one month apart 3. Elimination of all other possible diagnoses Various examinations are used for diagnosis, including a neurological exam, patient history, magnetic resonance imaging (MRI), cerebral spinal fluid (CSF) analysis, blood tests and evoked potential assessments. Neurological Exam: A complete neurologic examination is a critical diagnosis tool. Abnormal results suggestive of MS might include: yy Diffuse and highly variable hyperesthesia or anesthesia yy Irregularly distributed muscle weakness with spasticity VOLUME 1

yy Hyperreflexia yy Increase in deep tendon

reflexes yy Positive Babinski reflex yy Impaired or abnormal superficial reflexes yy Ataxia yy Uncoordinated speech yy Tremors yy Nystagmus yy Temporal pallor of the optic disks followed by optic atrophy yy Visual field defects yy Emotional lability MRI: An MRI provides high resolution images of cross sections of the brain and can demonstrate lesions, both old and active. Active lesions are shown with the uptake of a specific contrast material— gadolinium. Gadolium is injected at the time of the scan. The contrast will “light up” when a demyelination is occurring and lesions show up as paler areas. From an MRI, the neurologist can identify the presence and location of probable demyelination events, both of which can help explain the patient’s current symptoms and anticipate future manifestations. Currently, it is recommended that a first MRI be done as soon as a potential diagnosis is suspected, with follow-up MRIs to confirm.5,6 Typically a patient will have yearly MRIs to help determine if there is progression or evidence of new disease activity. This may prompt a change in treatment. Patients, for example, with more active disease may have an MRI ordered every six months

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to help determine response to therapy. CSF: A CSF sample is taken via a lumbar puncture (LP) along with a serum sample, looking for oligoclonal bands, indicative of immune system activity. A positive result is determined with oligoclonal bands in the CSF but not in the serum. An LP is positive in up to 95% of people with MS, but again is not specific to MS and other conditions must be ruled out. Evoked Potential Tests are performed to measure the size and speed of impulses along neurons. Weaker or slow signals indicate that demyelination has occurred and that MS is a possibility. There are three primary evoked potential tests: 1. V  isually Evoked Potential (VEP) measures the speed of the optic nerve. The patient focuses on the center of a "TV" screen on which there is a black and white checkered pattern. Each square in the pattern alternates between black and white at measured intervals. The patient wears a patch on one eye for a while and then on the other, so that the speed of both optic nerves can be measured. 2. B  rainstem Auditory Evoked Response (BAER) measures the speed of impulses along the auditory portion of Cranial Nerve VIII. The patient lies down in a darkened room to prevent the distraction of visual signals and a series of clicks and beeps are played back to the patient.

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3. SomatoSensory Evoked Potential (SSEP) involves strapping an electrical stimulus around an arm or leg. Low current is switched on for 5 seconds and electrodes on the back and skull measure the response at particular junctions. The speed of various nerves can be measured in this way and the points of slow-down (i.e. demyelinated lesions) approximated. Slow nerve responses in any of these tests are not necessarily indicative of MS but can be used in conjunction with a neurological examination, medical history, an MRI and a spinal tap to make a diagnosis.

Medication Therapies For MS The primary goals of therapy are to return a patient’s function after an attack, prevent new attacks and prevent or minimize disability. Therapy options differ depending on each patient’s stage and sub-type and for managing the various disease conditions. Early treatment is critical, ideally when neurologic examination results are normal. These therapies do not affect existing impairments; rather, they are aimed at preventing new clinical and radiologic activity and therefore help prevent recurrent attacks and the subsequent axonal loss that occurs early and is the cause of permanent neurologic disability. Even with appropriate use of medication, however, most patients with MS will suffer varying degrees of attacks and subsequent disability.

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Disease-modifying medications In order to impact disease progression, the activity of the immune system must be changed or modulated. Specific to MS, the goal is to reduce the lymphocytes that are active in MS—in terms of both numbers and movement into the CNS, i.e. the brain, spinal cord and optic nerves. Table 1 provides a summary of the currently available disease-modifying therapies (DMT), grouped by mechanism of action. Dimethyl fumarate (Tecfidera) works by decreasing inflammation

and blocking the ability of immune cells from entering the CNS. This drug is administered by mouth twice daily. Side effects may include flushing, stomach pain, diarrhea, nausea and vomiting, and heartburn.

a single episode as well as for relapsing-remitting multiple sclerosis. It is administered as a 20 mg subcutaneous injection a day. Side effects can include an injection site reaction in approximately one third of the patients, as well as typically mild flu-like symptoms in about 10% of users. A reaction that involves flushing, shortness in breath, anxiety and rapid heartbeat has been reported soon after injection in up to 5% of patients, typically subsiding within 30 minutes. A visible dent at the injection site can occur due to the local destruction of fat tissue, known as lipoatrophy or lypodystrophy.

Glatiramer acetate (Copaxone) is a combination of four amino acids (glutamic acid, lysine, alanine, and tyrosine) that are found naturally in myelin’s basic protein. This drug appears to work as a decoy for the immune system as it attacks the drug as opposed to the myelin. While clinical definition of multiple sclerosis requires two or more episodes of symptoms and signs, glatiramer acetate is approved for treatment after

Table 1: Summary of MS Therapies7 Brand Name

Route

Frequency

Efficacy

Safety

Tolerability

dimethyl fumarate

Tecfidera®

PO

BID

++

++

++

glatiramer acetate

Copaxone®

SC Inj

QD

+

++++

++

interferon beta-1a

Avonex® Rebif®

IM Inj SC Inj

QW 3xW

+

+++

+

pegylated interferon beta-1a

Plegridy™

SC Inj

Q2W

+

+++

+

Interferon beta-1b

Betaseron® Extavia®

SC Inj SC Inj

QOD QOD

+

+++

+

teriflunomide

Aubagio®

PO

QD

+

++

+++

Selective immunomodulation

Non-specific immunomodulation

Selective adhesion molecule inhibitor natalizumab

Tysabri®

Inf

Q4W

+++

+ (JC pos)

+++

natalizumab

Tysabri®

Inf

Q4W

+++

+++ (JC neg)

+++

Gilenya®

PO

QD

++

++

++

alemtuzumab

Lemtrada®

Inf

x5d initial dose; x3d one year later

++++

+

+

mitoxantrone

Novantrone®

Inf

Q3M

++

+

+++

S1P receptor modulator fingolimod Immunosuppression

PO=oral; Inj=injection; Inf=Infusion; SC=subcutaneous; IM=Intramuscular; JC=JC virus

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Interferons (IFNs) are proteins made and released by lymphocytes in response to a presenting antigen. They allow communication between cells activate the protective defenses of the immune system to rid the body of those foreign antigens. Interferons have a significant side effect profile, most frequently flu-like symptoms, increased body temperature, feeling ill, fatigue, headache, muscle pain, convulsion, dizziness, hair thinning, and depression. Erythema, pain and hardness at the injection site are common. And since IFN therapy causes immunosuppression, there is increased risk of infection. Some patients will not be able to tolerate these effects and will have to discontinue this specific therapy. Teriflunomide (Aubagio), a pyrimidine synthesis inhibitor, inhibits a key enzyme required by lymphocytes, thus reducing T cell and ultimately B proliferation. It also inhibits the production of immune messenger chemicals by T cells. Potential adverse reactions include nausea, diarrhea, thinning hair, and hepatotoxicity. This drug is also teratogenic and should not be taken by women who are pregnant or plan to become pregnant. Natalizumab (Tysabri) is an infused monoclonal antibody directed at lymphocytes. It is approved as single therapy for patients with RRMS to delay disease progression and reduce the rate of relapse. Second to mitoxantrone in terms of effectiveness, natalizumab is also well tolerated. There are, 6

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however, several potential serious adverse effects with natalizumab as well. Rare cases of progressive multifocal leukoencephalopathy (PML), a progressive demyelinating disease of the brain that typically causes permanent disability or death, were identified. The risk is higher in patients who receive other forms of immunotherapy, for example interferons or immunosuppressant medications, and thus the reason it is approved as monotherapy for MS patients. Less than 1% of the patients will develop hypersensitivity, in which case the natalizumab must be discontinued. As with the other immunomodulators, natalizumab also presents with the risk of infection. Because of the risk of PML, a restricted prescribing program, called the Tysabri TOUCH® prescribing program, is in place. Tysabri can only be prescribed, distributed and infused by prescribers, infusion centers and pharmacies with infusion centers that are registered in the program. Their commitment includes, for example, proof of patient education and consent, patient evaluation at three months, six months and then every six months after their first infusion. Then it is necessary to determine every six months if patients should continue on Tysabri and reauthorize if appropriate, and to report serious opportunistic and/or atypical infections. Patients must also be enrolled in the program and meet at the necessary conditions of the program.

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Fingolimod (Gilenya) prevents T-cells from getting out of the lymph nodes and into the circulation and, ultimately, into the CNS. It is given as a daily oral dose. While generally well tolerated, the risk of side effects is significant and patients should be monitored for liver dysfunction, macular edema (swelling of the central portion of the retina, causing distorted vision), elevated blood pressure, shortness of breath, bronchitis and diarrhea. Bradycardia was seen only upon first treatment; it is recommended that patients receive their first dose under medical supervision. Alemtuzumab (Lemtrada) is another infused monoclonal antibody. It targets a protein found on CD52 immune cells, likely binding with the CD52 on T and B cells and causing cellular lysis. This drug is initially administered for five consecutive days and then, one year later, for three consecutive days. Several serious adverse effects can occur. Patients are at risk for developing other autoimmune conditions such as immune thrombocytopenia or anti-glomerular basement membrane disease. Serious infusion reactions may occur. Patients also have an increased risk of developing certain cancers, including thyroid cancer, melanoma, and lymphoproliferative disorders and lymphoma. Because of these risks Lemtrada is only available through a restricted program called the LEMTRADA Risk Evaluation and Mitigation Strategy (REMS) Program, similar to the Tysabri Touch program.

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Mitoxantrone (Novantrone) is an immunosuppressant primarily used for MS in advanced RRMS and SPMS. It is arguably the most effective treatment option for MS, but limited in its use by severe dose-related cardiotoxicity and is therefore not considered as a long-term therapy. It is also potentially hepatotoxic. For patients placed on Mitoxantrone therapy, strict compliance with administration and monitoring guidelines is essential. Mitoxantrone is administered once every three months for a maximum of three years. A higher total dose increases the risk of serious heart damage. Patients must have an echocardiogram and a complete blood count prior to treatment to determine if the therapy is safe. Mitoxantrone should be discontinued at the first signs of heart damage, infection or liver dysfunction. Mitoxantrone is one of only two medicines that have been shown to benefit people who have secondary progressive MS that is relapsing. The other is the interferon beta medicine Betaseron. Interferon beta will likely remain the first choice for treating secondary progressive MS because it does not carry

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the risk of heart damage associated with mitoxantrone. There are also two non– disease-modifying therapies used with MS: yy High-dose corticosteroids are typically administered for acute exacerbations or relapses. Administered intravenously over three to five days, the goal is to accelerate recovery and minimize lasting deficits. Although generally effective in the short term for relieving symptoms, corticosteroid treatments do not appear to have a significant impact on disease progression. yy Dalfampridine (Ampyra®) is a potassium channel blocker used alone or with an immunomodulator. Blocking the potassium channels can improve the nerve conduction in affected nerves and dalfampridine improves walking speed. The approved dose is 10 mg, po, bid. Doses higher than 10 mg present a significant risk of seizure.

Use Of Multidisciplinary Treatments All of the existing diseasemodifying drugs ease

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symptoms but do not stop disease progression. As MS progresses, the symptoms tend to increase. For some, treatment efficacy is limited and the goal is symptom management. Given the potential range of deficits, most people with MS will need help from a variety of health professionals or services at some point. Neurologists are the main physicians involved. Treatments such as physiotherapy, speech and language therapy or occupational therapy can also help to manage some symptoms and maintain quality of life. Treatment of neuropsychiatric symptoms such as emotional distress and clinical depression should involve therapists, psychologists, and psychiatrists as appropriate. Neuropsychologists can help evaluate and manage cognitive deficits. Exercise, cognitive behavioral therapy and energy conservation should also be incorporated.t * Do not use the information in this article to diagnose or treat a health problem or disease without consulting a qualified physician. Patients should consult their physician before starting any course of treatment or supplementation, particularly if they are currently under medical care, and should never disregard medical advice or delay in seeking it because of something set forth in this publication.

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References 1. www.nationalmssociety.org/ About-the-Society/MS-Prevalance. Accessed July 7, 2015. 2. Pietrangelo A, Higuera V. Multiple Sclerosis by the numbers: facts, statistics, and you. www.healthline.com/ health/multiple-sclerosis/facts-statisticsinfographic. Published March 24, 2015. Accessed July 7, 2015. 3. Ciccarelli O, Toosy AT. Conversion from clinically isolated syndrome to multiple sclerosis: a large multicentre study. Mult Scler. 2015;21(8):967-968. 4. Kuhle J, Disanto G, Dobson R, Adiutori R, Bianchi L, Topping J. Conversion from clinically isolated syndrome to multiple sclerosis: a large multicentre study. Mult Scler. 2015;21(8):1013-1024.

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5. Anderson P. MRI guidelines in MS updated. Medscape Medical News from the Constorium of Multiple Sclerosis Centers (CMSC) 2015 Annual Meeting. Medscape reference. www.medscape.com/ viewarticle/845593?src+wnl_edit_ tpal&uac=5457FY#vp_1. Published May 29, 2015. Accessed June 1, 2015. 6. Polman CH, Reingold SC, Banwell B, Clanet M, Cohen JA, Filippi M, et al. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol.2011;69(2):292–302. 7. Krieger S, Bernard JT, Namey MA, Racke MK. Tried and true vs. new: weighing your MS treatment options CME/CE. Medscape reference. http://www.medscape.org/viewarticle/ 846315_transcript. Published June 26, 2015. Accessed July 7, 2015.

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Self-Assessment Quiz: Multiple Sclerosis LEARNING GOAL

LEARNING OBJECTIVES

Gain a general understanding of the immune processes involved in MS, the resulting clinical impact and its variability, and related treatment options.

After reviewing this publication, each participant should be able to: 1. Define adaptive immunity and the autoimmune process 2. Describe the specific autoimmune activity of multiple sclerosis and its clinical impact 3. Relay symptom characteristics and potential reasons for variation 4. Describe treatment options

SELF-ASSESSMENT QUESTIONS

In the Quiz Answers section on the next page, circle the correct answer for each question. To obtain two (2.0) contact hours toward CE credit, the passing score is 100%. Return your Self-Assesment Quiz to Coram via email, fax or mail. See the next page for details on how to return your quiz. Please allow approximately seven days to process your test and receive your certificate upon achieving a passing score. 1. With autoimmune disorders, the immune system develops a hypersensitivity response and reacts to normal body tissues. a. True b. False

7. Corticosteroids are the treatment of choice for long term maintenance to prevent recurrent attacks. a. True b. False

2. MS is an autoimmune process that results in destruction of the protective myelin of the: a. Central Nervous System b. Peripheral Nervous System c. A and B

8. Tysabri® is most effective when combined with an interferon therapy. a. True b. False

3. Symptoms of MS are consistent and progressive as myelin destruction occurs in an orderly fashion. a. True b. False 4. It is not uncommon for patients to reflect back on symptoms that may have indicated MS prior to their actual diagnosis. a. True b. False 5. Abnormal results suggestive of MS might include each of the following EXCEPT: a. Diffuse hyperesthesia b. Hyperreflexia c. Double vision d. Negative Babinski reflex

9. Relapsing/remitting MS presents as: a. A bout of symptoms often with complete recovery between exacerbations b. A progressive, predictable course with gradual disability c. An eventual progression of disability d. A and B e. A and C 10. Secondary progressive MS presents as a. Consistently district relapses and remission b. Limited long term symptoms or disability c. Relapses and remissions but, ultimately, incomplete symptom improvement and accumulating disability d. A and B e. C

6. An MRI can often identify the presence and location of demyelination events. a. True b. False 9

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