dallas, tx november 2–4, 2012 multiple sclerosis shirley o’leary ms np-c mscn texas neurology...
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![Page 1: Dallas, TX November 2–4, 2012 Multiple Sclerosis Shirley O’Leary MS NP-C MSCN Texas Neurology Dallas, Texas Mary L. Filipi APRN, PhD Neurology Associates,](https://reader035.vdocuments.us/reader035/viewer/2022081603/56649e0b5503460f94af39f0/html5/thumbnails/1.jpg)
Dallas, TX • November 2–4, 2012
Multiple SclerosisShirley O’Leary MS NP-C MSCN
Texas Neurology
Dallas, Texas
Mary L. Filipi APRN, PhD
Neurology Associates, PC.
Lincoln, NE
Assistant Professor – College of Nursing
University of Nebraska Medical Center
Omaha, NE
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Dallas, TX • November 2–4, 2012
MULTIPLE SCLEROSIS
Autoimmune CNS disease
T-cell mediated
Progressive/Degenerative
Unpredictable course
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Dallas, TX • November 2–4, 2012
Pathology
Characterized by inflammation and demyelination of white matter or myelinated fibers of brain and spinal cord.
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Dallas, TX • November 2–4, 2012
Multiple Sclerosis
• Inflammatory & degenerative disease of the central nervous system (CNS) that destroys myelin, oligodendrocytes, axons
• Inflammation may have a dual role in MS: tissue damage and neuroprotection
• Affects >1 million individuals in North America and Europe
• Major cause of nontraumatic neurological disability in young adults
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Dallas, TX • November 2–4, 2012
Disease Progression
• Clinical course is variable
• Early disease may be subclinical (asymptomatic)
• Pathogenesis of MS is not fully understood
• MS may be a single disease or a common endpoint of multiple disease etiologies
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Dallas, TX • November 2–4, 2012
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Dallas, TX • November 2–4, 2012
ETIOLOGY
• Autoimmunity– Genetic predisposition– Environmental factors
• Infection– Molecular mimicry (herpes simplex,
Chlamydia).
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Dallas, TX • November 2–4, 2012
MS PATHOLOGY
• Disease of CNS white matter• Multifocal areas (plaques) of axonal
demyelination– Moderate loss of axons– Loss of oligodendrocytes– Astroglial scaring
• Demyelination of axons can reduce speed or block nerve impulses
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Dallas, TX • November 2–4, 2012
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Dallas, TX • November 2–4, 2012
Demyelination and Axonal Transection
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Dallas, TX • November 2–4, 2012
MOST COMMON SYMPTOMS OF MULTIPLE SCLEROSIS• Pyramidal weakness 45%
• Optic neuritis 40%
• Sensory loss 35%
• Brainstem dysfunction 30%
• Cerebellar ataxia and tremor 25%
• Cognitive impairment 34-65%
• Sphincter disturbances 20%
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Dallas, TX • November 2–4, 2012
MS
Abnormal immune response to one or more myelin antigens that occur in genetically susceptible persons after exposure to an as yet undefined casual agent (Hauser)
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Dallas, TX • November 2–4, 2012
DIAGNOSTIC CRITERIAPoser – dissemination in time and place
based on history and neurological examination
McDonald – combination of MRI and clinical finding to document dissemination
- at least one clinical event required
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Dallas, TX • November 2–4, 2012
DIAGNOSIS
Brain MRI is commonly over interpreted
Diagnosis of MS must be based on clinical findings and MRI information
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Dallas, TX • November 2–4, 2012
Incr
easi
ng
dis
abili
ty
Time
What Course Might MS Take Over a Lifetime?
• MS can progress differently in different people• The disease may be a combination of relapses, recovery,
and progression
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Dallas, TX • November 2–4, 2012
MAJOR CLINICAL COURSES OF MS
5%5%
50%50%
30%30%
15%15%
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Dallas, TX • November 2–4, 2012
Clinical Disability in MS
5 10
Years
15 20
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Dallas, TX • November 2–4, 2012
M R I
Plaques found: periventricular regions, corpus callosum, brainstem, cerebellum and spinal cord.
Hyperintense on T2 and FLAIR sequences sometimes hypointense (black holes) on T1
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Dallas, TX • November 2–4, 2012Wingerchuk DM, et al. Lab Invest. 2001;81:263-281.
Pathophysiologic Features of MS
• Pathological signature of MS is the white matter (WM) circumscribed areas of demyelination
• Lesions may occur anywhere in WM but are most commonly seen in– Periventricular regions– Optic nerves– Brain stem– Cerebellum– Spinal cord
• Lesions may contain varying proportions of immune cells and immunoreactive substances depending on stage of the disease
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Dallas, TX • November 2–4, 2012
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Dallas, TX • November 2–4, 2012
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Dallas, TX • November 2–4, 2012
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Dallas, TX • November 2–4, 2012
The Importance of Early Treatment
Treatment at diagnosis
Later treatment
Disease Onset
Based on theoretical model
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Dallas, TX • November 2–4, 2012
TREATMENTS
•Disease modifying agents – CRAB’s•Symptomatic treatment•Treatment of acute relapses
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Dallas, TX • November 2–4, 2012
PEARLS OF MS TREATMENTAll symptoms are not MS related
↑ core temperature
↑ symptoms
40% of flares are pseudo flares
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Dallas, TX • November 2–4, 2012
Fatigue
Fatigue is the major debilitating factor in
MS
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Dallas, TX • November 2–4, 2012
IV Disease and Flare Treatment
• Solumedrol 1 gram IV in 250 NS to run 4-6 hrs – may follow with a minimal oral taper
• Tysabri 300 mg IV in 100 cc NS to run over 1 hour with a one hour wait following infusion – NO EXCEPTIONS
• Alemtuzumab 12 mg in 100 cc NS or 5% glucose over 4 hours for first dose 3rd & 4th dose over 2 hours minimum, 8 hours maximum
![Page 28: Dallas, TX November 2–4, 2012 Multiple Sclerosis Shirley O’Leary MS NP-C MSCN Texas Neurology Dallas, Texas Mary L. Filipi APRN, PhD Neurology Associates,](https://reader035.vdocuments.us/reader035/viewer/2022081603/56649e0b5503460f94af39f0/html5/thumbnails/28.jpg)
Dallas, TX • November 2–4, 2012
Tysabri
• 300 mg IV q 28 days to run over 1 hour or more• Mix gently invert bag to mix• Stable for 8 hours• May premedicate with Tylenol, Zantac, and
antihistamine• Premedication may include Solu-Medrol• Must be enrolled in TOUCH prescribing
program
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Dallas, TX • November 2–4, 2012
Alemtuzumab
• IV over 4 hours for first 2 doses – 5 days annually
• Premedicate with methylprednisolone, tylenol, diphenhydramine, cetirizine hydrochloride, odansetron and famotidine
• During infusion – tylenol, odansetron and naprelan
• Post infusion - famotidine
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Dallas, TX • November 2–4, 2012
Alemtuzumab
• Thyroid problems
• ITP
• Will need long term monitoring
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Dallas, TX • November 2–4, 2012
Questions