What is the allele for the genetic predisposition and how much higher of a risk do they have?
HLA-DRB1501 MHC class 2 allele 3X higher risk for MS
What do the majority of patients present with?
85%: Relapsing remitting symptoms (RRMS). Remainder 15% present with progressive relapsing or primary progressive MS.
What are the signs and symptoms of MS (there are 9)
Focal weakness:
-UMN pattern of weakness
Focal numbness/paresthesias:
-Tingling, band like sensation around abdomen
Optic neuritis
-Painful inflammation of the optic nerve
Speech difficulties:
Lhermitte’s:
-Flexion of the neck results in parasthesiae (cervical cord demyelination)–>electrical sensation that runs down the back and into the limbs
Uhthoff’s:
-Symptoms exacerbated by overheating, reduces conduction due to lack of myelin
Coordination/gait/balance:
Spasticity:
-Esp in legs
Urinary symptoms:
Gadolinium
Does not cross the BBB. If you have a gadolinium enhancing lesion, that means your BBB is breaking down. MS lesions do not respect vascular territory
How is the BBB disrupted in MS
Perivascular inflammatory infiltration (T cells=driving force) secrete cytokines which disrupt capillary barriers
MRI findings in MS (there are 6)
Gadolinium-enhancing lesion
- Frequent in subclinical phase
- Usually resolve
White matter lesion
- Myelin loss
- Often in corpus callosum in MS
Black holes
- Glial scar from myelin loss (SPMS correlation)
- Chronic MS lesions
Dawson’s fingers
-Seen on FLAIR image. Periventricular demyelination
Brain atrophy
-Occurs early and progresses
Spinal cord lesion
-Sensory complaints, loss of upper coordination, ambulatory difficulties
Oligoclonal bands
IgG bands in the CSF, non specific for MS, but 80-90% of MS pts will have it
MS treatments
- Treat or remove inciting agents of stimulus
- stress, infection - Mild
- observe, reassurance, treat symptoms - Moderate/Severe
- IV steroids, PT, treat symptoms
Everyone should always be on a treatment, stops progression
- Type I intereferon (Avonex, Rebif, Betaseron)
- Glatiramer acetate (copaxone)
What are the key steps in MS neurophatogenesis
- CNS entry of activated T cells, monocytes
- Neuroinflammation
- Axonal degeneration
What are the classic clinical features of MS
Waxing and waning long tract signs occurring over weeks/months (motor, sensory, coordination etc)
