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14 Cards in this Set

  • Front
  • Back
Multiple Sclerosis
-CNS condition involving UMN's
-autoimmune demyelination disease of the spinal cord and brain
-second leading cause of disability in young people; age of onset is 20-30
-usually first presents with optic neuritis, then progression to UMN deficits
-relapse is common(new neurological deficit that appears in pt); corresponds to a new MS attack as a result of a new lesion
LMN Signs
-weakness, atrophy, decreased tone, areflexia, fasciculations
UMN Signs
-characteristic of MS
-weakness, spasticity, increased tone, hyperreflexia, Babinski sign
Classic MS Patient
-acute optic neuritis
-evidence of active and past lesions on MRI of the brain(MRI is essential for diagnosis)
-positive oligoclonal bands
Another classic MS patient
-partial transverse myelitis
-evidence of past lesions on MRI of the brain
-evidence of optic neuritis
-pt exhibits separation of time and space of symptoms
MS Classifications
1. Primary Progressive
2. Relapsing Remitting
Primary Progressive MS
-around 10-15% of patients
-very cumulative from the beginning
-first occurrence, have a relapse and dont get much better, and continue to get worse with each relapse
-more often seen in young men
Relapsing Remitting MS
-about 85% of patients
-pts are fine, relapse, recover, relapse, recover, etc
-may have a few lingering defects such as afferent pupil defect, but they remain functional
-after about 10-15 yrs, pt will get into an area of secondary progression -> no new lesions, just getting worse
Causes of MS
-T Cells
-Genetics
-Low Vitamin D
-Eppstein-Barr virus
T Cells
1. Auto-reactive T cells - attack myelin
2. T cell imbalance
-TH1: pro-inflammatory; elevated levels, *therapy seeks to lower T1:T2 ratio
-TH2: anti-inflammatory; treatment aims to increase these
3. MS Plaque - myelin loss seen as a light area in imaging**
Genetics
-30% MS risk
-2 DRB-150 copies increase risk
-first autoimmune disease shown to have genetic linkage to HLA
Vitamin D
-studies report lower Vit D levels in MS pts
-higher incidence of MS at higher altitudes-> correlates to vit D influence(possibly from less sun exposure)
First line drugs
1. Interferon B: was first drug on market; has multiple effects; injectable; causes flu-like symptoms; increases TH2 count
2. Glatiramer acetate: subcutaneous injection that is given daily; is an amino acid compound that mimics myelin protein; causes alteration in immunity, pts do not have relapse; increases TH2 count; no flu-like symptoms
3. Fingolimod: first oral treatment; derived from myriocin(fungus); blocks Sphingosine-1-phosphate receptors(keeps activated T cells from egressing from the lymph nodes)
Second line drugs
1. Tysabri: strongest MS drug; prevents active T cells from crossing the blood/brain barrier; pts on the drug for a long time have been shown to develop Progressive Multifocal Leukoencephalopathy (PML)...life-threatening
2. Mitoxantrone: only used when pt is degrading rapidly and has failed other treatments; very toxic