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Multiple Sclerosis

Multiple Sclerosis. Charity, Scott, Natalia. Unless otherwise noted all information was obtained via National MS Society and National MS Society WA Chapter. Multiple Sclerosis Mystery. MS is thought to be an autoimmune disease Affects CNS

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Multiple Sclerosis

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  1. Multiple Sclerosis Charity, Scott, Natalia Unless otherwise noted all information was obtained via National MS Society and National MS Society WA Chapter

  2. Multiple Sclerosis Mystery • MS is thought to be an autoimmune disease • Affects CNS • Triggers are unknown, but research is focusing in on viruses, environmental, and genetic factors • Antibody titers to many viruses are elevated in MS patients. • Varicella zoster, vaccinia, rubella, Epstein-Barr, HHV-6 • HHV-6 antibodies have been detected near brain lesions characteristic of MS

  3. FACTORS & INFLUENCES • Age of diagnosis usually 20 to 50 • Patients have been as young as 2 and as old as 75 • Environment • NW has a higher incidence • Predominant in cooler climates and areas further from the equator • Vitamin D may play a role • Genetic Factors • 2-3 times more likely in females than males • Variable among races and ethnicities • Highest in northern European Caucasians • Lowest in Asians • No particular gene has been identified – likely multiple genes are involved

  4. PATHOPHYSIOLOGY • Key players • Axons • Myelin • Oligodendrocytes • Blood vessels that supply oxygen and nutrients • Cytokines • T-cells • Antigen-presenting cells (APCs)

  5. PATHOPHYSIOLOGY • During immune response cells identify antigens and interpret components of myelin as foreign • APC cells present myelin antigen to T-cells • T-cells pass through blood brain barrier (BBB) • Normal BBB prevents passage of potential harmful substances through blood vessel walls within brain • MS patients’ BBB ‘springs a leak’ • Allows activated T-cell to cross BBB and mount attack on myelin • This leads to several events that lead to demyelination • Swelling • Activation of macrophages • More activation of cytokines

  6. PATHOPHYSIOLOGY • Demyelination • Information transmission via axon is interrupted • Interferes with conduction of nerve impulses from sensory organs to CNS and from CNS to muscles • May result in permanent loss of neuron transmission • Remyelination – repair process • Myelinating oligodendrocytes are able to rebuild thinner, less effective myelin sheaths • May be reason symptoms decrease of temporarily disappear during early part of disease • There is still irreversible loss and nerve damage

  7. Courtesy of Multiple Sclerosis Research Australia

  8. SYMPTOMS • Symptoms are unpredictable and vary • Fatigue – 90% • Depression – 70% • Suicide 7.5 times higher • Motor involvement – muscle weakness, numbness • Visual symptoms – blurring, twitching of eyes • Cerebellar involvement – intention tremor, seizure • Genitourinary symptoms – constipation, urine frequency • Cognitive defects – short-term memory dysfunction

  9. TREATMENTS • No cure for MS • Treatment focused on relief of symptoms and slowing progression • Patient response to disease and treatment will differ • Corticosteroids – most common • Methylprednisolone IV and prednisone • Decrease intensity of body’s defense reaction • Prevent damage to BBB

  10. TREATMENTS • Interferons • Beta 1-a: Avonex and Rebif • Anti-inflammatory properties • Beta 1-b: Betaseron • Diminish activity of specific WBCs causing disease • Glatiramer acetate • Believed to modify immune process that causes MS

  11. TREATMENTS • Psychotherapy • PT/OT/ST • STICK TO TREATMENT PLAN!

  12. PROGNOSIS • Life expectancy ~35 years after onset • Relatively normal life • After ~25 years, 2/3 remain mobile • Eventually leads to physical limitations for ~70% of patients

  13. KEY FEATURES OF MS • Thought to be an autoimmune disease affecting CNS • Involves myelin damage that interrupts nerve conduction • No cure – treatment focused on comfort and slowing progression • Response to disease and treatment will vary among patients

  14. ?? QUESTIONS ??

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