Transcript The Many Faces of Multiple Sclerosis
Multiple Sclerosis
Shirley 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
Dallas, TX • November 2–4, 2012
MULTIPLE SCLEROSIS
Autoimmune CNS disease T-cell mediated Progressive/Degenerative Unpredictable course Dallas, TX • November 2–4, 2012
Pathology
Characterized by inflammation and demyelination of white matter or myelinated fibers of brain and spinal cord.
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
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
Dallas, TX • November 2–4, 2012
Dallas, TX • November 2–4, 2012
ETIOLOGY
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Autoimmunity
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Genetic predisposition
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Environmental factors
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Infection
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Molecular mimicry (herpes simplex, Chlamydia).
Dallas, TX • November 2–4, 2012
MS PATHOLOGY
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Disease of CNS white matter Multifocal areas (plaques) of axonal demyelination
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Moderate loss of axons Loss of oligodendrocytes Astroglial scaring Demyelination of axons can reduce speed or block nerve impulses Dallas, TX • November 2–4, 2012
Dallas, TX • November 2–4, 2012
Demyelination and Axonal Transection
Dallas, TX • November 2–4, 2012
MOST COMMON SYMPTOMS OF MULTIPLE SCLEROSIS
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Pyramidal weakness Optic neuritis Sensory loss Brainstem dysfunction Cerebellar ataxia and tremor Cognitive impairment 65%
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Sphincter disturbances 45% 40% 35% 30% 25% 34 20% 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) Dallas, TX • November 2–4, 2012
DIAGNOSTIC CRITERIA
Poser – 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 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 Dallas, TX • November 2–4, 2012
What Course Might MS Take Over a Lifetime?
Time
• MS can progress differently in different people • The disease may be a combination of relapses, recovery, and progression
Dallas, TX • November 2–4, 2012
MAJOR CLINICAL COURSES OF MS
5% 50% 30% 15%
Dallas, TX • November 2–4, 2012
Clinical Disability in MS
5 10 Years 15 20 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 Dallas, TX • November 2–4, 2012
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
Dallas, TX • November 2–4, 2012 Wingerchuk DM, et al. Lab Invest. 2001;81:263-281.
Dallas, TX • November 2–4, 2012
Dallas, TX • November 2–4, 2012
Dallas, TX • November 2–4, 2012
The Importance of Early Treatment
Later treatment Treatment at diagnosis Disease Onset Based on theoretical model Dallas, TX • November 2–4, 2012
TREATMENTS
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Disease modifying agents – CRAB’s
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Symptomatic treatment
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Treatment of acute relapses Dallas, TX • November 2–4, 2012
PEARLS OF MS TREATMENT
All symptoms are not MS related
↑ core temperature ↑ symptoms 40% of flares are pseudo flares
Dallas, TX • November 2–4, 2012
Fatigue
Fatigue is the major debilitating factor in MS
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 3 rd & 4 th dose over 2 hours minimum, 8 hours maximum
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
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
Dallas, TX • November 2–4, 2012
Alemtuzumab
• Thyroid problems • ITP • Will need long term monitoring
Dallas, TX • November 2–4, 2012
Questions
Dallas, TX • November 2–4, 2012