Dallas, TX November 2–4, 2012 Multiple Sclerosis Shirley O’Leary MS NP-C MSCN Texas Neurology...

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


MULTIPLE SCLEROSIS

Autoimmune CNS disease

T-cell mediated

Progressive/Degenerative

Unpredictable course


Pathology

Characterized by inflammation and demyelination of white matter or myelinated fibers of brain and spinal cord.


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


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


ETIOLOGY

• Autoimmunity– Genetic predisposition– Environmental factors

• Infection– Molecular mimicry (herpes simplex,

Chlamydia).


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


Demyelination and Axonal Transection


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%


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)


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


DIAGNOSIS

Brain MRI is commonly over interpreted

Diagnosis of MS must be based on clinical findings and MRI information


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


MAJOR CLINICAL COURSES OF MS

5%5%

50%50%

30%30%

15%15%


Clinical Disability in MS

5 10

Years

15 20


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, 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


The Importance of Early Treatment

Treatment at diagnosis

Later treatment

Disease Onset

Based on theoretical model


TREATMENTS

•Disease modifying agents – CRAB’s•Symptomatic treatment•Treatment of acute relapses


PEARLS OF MS TREATMENTAll symptoms are not MS related

↑ core temperature

↑ symptoms

40% of flares are pseudo flares


Fatigue

Fatigue is the major debilitating factor in

MS


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


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


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


Alemtuzumab

• Thyroid problems

• ITP

• Will need long term monitoring


Questions

Dallas, TX November 2–4, 2012 Multiple Sclerosis Shirley O’Leary MS NP-C MSCN Texas Neurology...

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