Transcript Document
Multiple Sclerosis (MS) Program
Epidemiology/Demographics
Pathophysiology
Clinical course
Symptoms
Diagnosis
Treatment options
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Multiple Sclerosis
Overview
Chronic, inflammatory, demyelinating disease
Affects the myelin sheath and axons of the Central
Nervous System (CNS)
Progressive clinical course
Common cause of disability
in young adults
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Epidemiology
• Prevalence varies around the world
• Greater frequency in higher latitudes (above
40° latitude) than in lower latitudes
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•
•
Two to three times more common in women
350,000 to 500,000 people in U.S.
The average person in the United States has about
one chance in 750 of developing MS
Sources: http://www.msfacts.org/info/info_faq.html and http://www.nationalmssociety.org/Sourcebook-Epidemiology.asp. Accessed May 9, 2006.
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Demographic Factors
Age
Onset: 15 to 50 years of age
Peak onset: between 20 and 30 years of age
Onset rare before age 10 or after age 60
Gender
More common in females
- 3:1 female versus male
Race
Incidence higher in Caucasians
Sources: http://www.msfacts.org/info/info_faq.html, http://www.ninds.nih.gov/disorders/multiple_sclerosis/detail_multiple_sclerosis.htm#54263215 and
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http://www.nationalmssociety.org/Sourcebook-Epidemiology.asp. Accessed May 17, 2006.
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Is MS a Hereditary Disease?
Genetic factors
First- and second-degree relatives are at
increased risk
Risk is higher in siblings
- Nontwin siblings (2%)
- Monozygotic twins (30%)
- Dizygotic twins (2.3%)
Susceptibility gene
Major histocompatibility
complex (MHC) on
chromosome 6
Source: http://www.msfacts.org/info/info_faq.html, http://www.ninds.nih.gov/disorders/multiple_sclerosis/detail_multiple_sclerosis.htm#54263215 and
http://www.nationalmssociety.org/Sourcebook-Epidemiology.asp. Accessed May 17, 2006
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Effects of Demyelination and
Axonal Damage
Loss of myelin and axonal damage may lead to:
Conduction block at the site of myelin/axonal loss
Slowed motor and sensory impulses in areas of
disease activity, resulting in compromised sensation
or movement
Increased subjective fatigue (greater energy
consumption)
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Signs and Symptoms
Depend on clinical course and disease progression
Vary based on lesion location
Exacerbated by heat and stress
Secondary complications due to underlining
neurological dysfunction
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Signs and Symptoms of MS
by Lesion Location
Optic nerve
Monocular visual loss
Scotoma
Spinal cord
Limb weakness
Spasticity and
hyper-reflexia
Lhermitte’s sign
Urinary urgency and
incontinence
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Signs and Symptoms of MS
by Lesion Location
Brainstem
Diplopia (double vision)
Pain (acute versus chronic)
- Trigeminal neuralgia, tic-like
extremity pain
- Aching back pain, burning
sensation, leg spasms
Numbness of face and
tongue
Vertigo (sensation of moving
around in space)
Nystagmus (involuntary eye
movements)
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Signs and Symptoms of MS
by Lesion Location
Cerebrum
Impairment of
concentration or memory
Hemiparesis (unilateral
paralysis)
Hemisensory loss
Visual field defect
Cerebellum
Incoordination of limbs
Ataxic gate
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Signs and Symptoms of MS
Severe fatigue
Experienced by 75% to 95% of MS sufferers
Depression
Etiology can be a:
- Symptom
- Secondary complication
- Side effect of medications
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Secondary Complications
Depression
Urinary tract infection
Accelerated lumbar spondylosis
Aspiration pneumonia
Pulmonary thromboembolism
Pressure sores
Limb contractures
Gastroparesis
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What is an Exacerbation?
Neurological attacks or aggravation of symptoms
Indicative of a new immune attack on myelin
Should last at least 24 hours
Untreated attacks, can last from weeks to months
(resulting in slow recovery/residual effects)
Precipitating factors can be identified
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Precipitating Factors
for Exacerbations
Fever (most common), infections – especially
urinary tract infections – without fever
Heat sensitivity
Emotional stress
Physical exertion
Fatigue
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Diagnosis
Clinical findings
History
Neurologic exam
Clinical picture
Laboratory evaluations
Magnetic resonance
imaging (MRI)
Evoked potentials
Cerebrospinal fluid
(CSF) analysis
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Diagnosis
Lesions disseminated in time and space
Time: More than one attack separated by
at least one or two months
Space: CNS involvement of more than
one area
Exclusion of other possible causes
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Diagnosis:
History
Signs and symptoms
Frequency of occurrence
Relapsing/remitting pattern
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Diagnosis:
Neurological Exam
Cerebral (mental)
Pyramidal (motor)
Sensory
Bowel and bladder
Brain stem
Visual/Optic
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Diagnosis:
MRI
Highly sensitive in detecting MS lesions of the
brain and spinal cord
Evidence of dissemination of lesions in time
and space
Helpful in excluding other causes, such as tumors
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Diagnosis:
Evoked Potentials
Measure nerve conduction velocity
Visual
Brainstem auditory
Somatosensory
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Diagnosis Cerebrospinal
Fluid Analysis
Immune abnormalities
Increased intrathecal Immunoglobulin G (IgG)
synthesis with oligoclonal bands present
Increased inflammatory cytokines -- such as,
interferon gamma (IFN-y) -- TNF and interleukin 2
(IL-2)
Increased activated CD4+ T cells
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Clinical Course:
Relapsing-Remitting (RRMS)
Most common type of MS
Signs and symptoms evolve over several days
Spontaneous improvement or in response to
corticosteroids
Full recovery or some residual deficit upon
recovery
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Clinical Course:
Secondary Progressive (SPMS)
Initially begins as relapsing-remitting MS
Progressive deterioration with or without relapses
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Clinical Course:
Primary-Progressive (PPMS)
Progressive deterioration without relapses
and remissions
Occasional plateaus and temporary
minor improvements
Tends to occur in older people
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Clinical Course:
Progressive-Relapsing (PRMS)
Rare
Progressive course from the onset
Acute relapses that may or may not result in
complete recovery
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Progression
Relapsing-remitting to secondary progressive
30% to 40% within six years to 10 years of onset
58% within 11 years to 15 years
90% after 25 years
Disability progression
8 years to moderate disability
15 years to severe disability
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Factors Affecting Prognosis
Favorable
Low attack rate
Long interval to second
attack
Complete recovery from
first attack
Younger age at onset
Female sex
Low disability at 2 and 5
years
Unfavorable
High attack rate
Short interval to second
attack
Lack of recovery from
first attack
Older age at onset
Early cerebellar
involvement
Insidious motor onset
Early development of
mild disability
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Evaluating Disability in MS
Functional systems (FS):
Pyramidal, cerebellar, brain stem, sensory, bowel
and bladder, visual, cerebral, and other
Each FS is independent of each other
Grading:
- Pyramidal, sensory, bowel and bladder, visual (0-6)
- Cerebellar, brain stem, cerebral (0-5)
- Other (0 or 1)
Scores are not additive
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Evaluating Disability in MS (cont.)
Expanded disability status scale (EDSS)
Consists of 20 steps from 0 (normal) to 10 (death due
to MS). Half-steps are included.
Gain/loss of 0.5 steps defines disease
improvement/worsening
Ordinal (rank scale)
Relies on standard neurologic examination
(FS assessment)
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Treatment Goals
Reduce (control) relapses
Delay disease progression
Delay disability
Alleviate symptoms
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Early Treatment
The National MS Society recommends:
“Initiation of therapy with an immunomodulator is
advised as soon as possible following a definite
diagnosis of MS with a relapsing course, and may be
considered for selected patients with a first attack
who are at high risk for MS.”
Source: Recommendation of the Executive Committee of the Medical Advisory Board of the Nat’l MS Society
www.nationalmssociety.org/Sourcebook-Early.asp. Accessed May 17, 2006.
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Current Therapies:
Immunosuppressants and Immunomodulators
Corticosteroids
Interferons :
Betaseron (interferon -1b)
Avonex (interferon -1a)
Rebif (interferon -1a)
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Current Therapies: (cont.)
Immunosuppressants and Immunomodulators
Immunosuppressants and immunomodulators:
cornerstone of therapy (cont.)
Copaxone (glatiramer acetate)
Novantrone (mitoxantrone)
Symptomatic management
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Corticosteroids
Symptomatic management
Used in moderate-to-severe exacerbations
IV methylprednisolone 500 mg/day for five days
followed by oral prednisone (optional)
Hasten clinical recovery
Delay recurrence of neurologic events
Does not alter the course of MS
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Interferon Beta
Mechanism of Action
Reduce the production of the TNFa (tumor
necrosis factor alpha) and T-cells, known to induce
damage to myelin
Reduce inflammation by:
Switching cytokine production from type 1 (proinflammatory) to type 2 (anti-inflammatory) cells
Increasing levels of interleuken 10 (IL-10)
Decrease antigen presentation, to reduce the
attack on myelin
Reduce the ability of immune cells to cross the
blood-brain barrier, by affecting adhesion
molecules, chemokines, and proteases
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Interferons :
Avonex (Interferon -1a)
Indication: relapsing
Avonex-lyo-vial
forms of MS
Dose: 30 mcg IM
once weekly
Reduces rate of
clinical relapse
Reduces the development
of new lesions
Delays the increase in
the volume of lesions
May delay progression
of disability
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Interferons :
Rebif
Interferon -1a
Indication: relapsing/remitting forms of MS
Dose: 22 or 44 mcg SC 3 times per week
Decreases frequency of relapse
Delays the increase in the
volume of lesions
May delay progression
of disability
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Interferons :
Betaseron (interferon beta-1b)
Indication: Relapsing forms of MS
Dose: 8 million IU SC every other day
Reduces rate of clinical relapse
Reduces the development of
new lesions
Delays the increase in the
volume of lesions
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Side Effects of Interferons
Common:
Flu-like symptoms
Chills
Fever
Muscle aches
Asthenia (weakness)
Betaseron and Rebif
have injection site
reactions
Uncommon:
Severe depression
Suicide
Seizures
Cardiac effects
Anemia
Elevated liver enzymes
Severe hepatic injury,
including cases of
hepatic failure, has been
reported in patients
taking Avonex
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Noninterferons:
Copaxone (glatiramer acetate) PFS
Indication: Reduction of frequency of relapses in
patients with RRMS
Dose: 20 mcg SC once daily
Reduces the frequency of exacerbations
Moderately reduces the
development of new lesions
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Copaxone Mechanism of Action
Synthetic chain of four amino acids
Structurally resembles the myelin basic protein
molecule
Believed to block the immune system from
attacking myelin
Switches the immune response from TH-1 cells
(pro-inflammatory) to TH-2 cells (anti-inflammatory)
which could reduce myelin damage
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Copaxone:
Side Effects
Common
Injection site reactions
Chest pain (transient –
20 to 30 minutes – not
life threatening but very
scary)
Uncommon
Nausea
Vomiting
Dizziness
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Auto Injectors
autoject® 2 for glass syringe
Dispenses Copaxone
Rebiject®
Dispenses Rebif
autoject® 2.25
Dispenses Betaseron
All provided free from manufacturer.
Rebiject and Copaxone need a prescription.
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Antineoplastics:
Novantrone (mitoxantrone)
Indication: Reduction of
relapse rate and clinical
disability in patients with
SPMS, PRMS or
worsening RRMS
Dose: 12 mg/m2 as short
IV infusion (five minutes
to 15 minutes every three
months)
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Antineoplastics:
Novantrone (cont.)
Reduces exacerbation rate
Prolongs time to first treated relapse
Improves EDSS scores versus baseline
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45
Novantrone
Mechanism of Action
Inhibits or prevents the development of any
uncontrolled new or abnormal growth, such as a
neoplasm or tumor
Suppresses B-cell and T-cell immunity
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Novantrone
Side Effects
Moderate to severe
Bone marrow suppression
- Neutropenia (decreased WBC and ANC)
- Thrombocytopenia (decreased platelets)
- Acute myelogenous leukemia
Cardiac toxicity
- Congestive heart failure (CHF)
- Decreased left ventricular ejection fraction (LVEF)
- Maximum cumulative dose 140 mg/m2
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Novantrone
Side Effects
Moderate to severe
Teratogenic effects
- Fetal growth retardation in rats
- Shortened gestation period
- Excreted in breast milk
Mild to moderate
Increased liver enzymes
Nausea
Alopecia (hair loss - transient)
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Novantrone
Contraindications
LVEF < 50%
CHF
Baseline neutrophil count < 1500 cells/mm3
Pre-existing myelosuppression
Abnormal LFT
Pregnancy, breastfeeding
Cumulative lifetime dose 140 mg/m2
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Immunosuppressants
Show only slight evidence of benefit in MS
Used only for progressive MS
Associated with serious side effects
Thiopurines (Imuran)
Methotrexate
Alkylating agents (Cytoxan)
Cyclosporine
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Symptomatic Treatments
Problem
Symptoms
Management
Spasticity
Painful spasms in the
lower and upper limbs
Remove irritating factors
Physical therapy,
baclofen, diazepam,
dantrolene
Paroxysmal phenomena
Trigeminal neuralgia,
pain, tonic seizures
carbamazepine,
Neurontin, phenytoin
Fatigue
Feeling tired (morning or
early afternoon)
Energy conservation,
amantidine
Depression
Common, occurs in high
percentage of patients
Anti-depressants
Sexual dysfunction
Inability to produce/
sustain an erection
Behavioral therapy
Viagra, Muse
Urinary dysfunction
Urgency, frequency and
retention
Detrol, Ditropan, Botox
Note, some of the drugs listed are shown for off-label use.
This page contains prescription brand drugs that are registered or registered trademarks of pharmaceutical manufacturers that are not affiliated with Caremark.
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Conclusion
Early treatment may delay disability and enhance
recovery from relapses
Treatment must be a cooperative effort between
multidisciplinary team of healthcare providers
Medications are not a cure for MS
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Challenges
Challenges for the person with MS
Physical difficulties
Financial concerns
Social issues
Emotional issues
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Resources and Links
Support/Information
National MS Society (NMSS) 1-800-FIGHT-MS
Consortium of MS Centers 1-201-837-0727
MS Foundation 1-800-441-7055
MS Association of America 1-800-833-4MSA
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Resources and Links
Copaxone - Shared Solutions®, 1-800-887-8100
www.copaxone.com
www.mswatch.com
www.MSuniversity.com
Rebif – MS LifeLines™, 1-877-44-REBIF
www.rebif.com
www.mslifelines.com
Avonex – MS Active SourceSM, 1-800-456-2255
www.avonex.com
www.MSactivesource.com
Caremark does not operate the Web sites/organizations listed here, nor is it responsible for the availability or reliability of their content. These
listings do not imply or constitute an endorsement, sponsorship or recommendation by Caremark.
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Resources and Links
Betaseron - MS PathwaysSM, 1-800-788-1467
www.betaseron.com
www.MSpathways.com
Novantrone, 1-877-447-3243
www.novantrone.com
www.MSlifelines.com
Caremark does not operate the Web sites/organizations listed here, nor is it responsible for the availability or reliability of their content. These
listings do not imply or constitute an endorsement, sponsorship or recommendation by Caremark.
Caremark proprietary and confidential information. Not for distribution.
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