Multiple Sclerosis

immune response attacks what 3 things

myelin, oligodendrocytes, nerve fibers

in what stage MS can oligodendrocytes survive and can reproduce myelin

early

what cannot occur once oligodendrocytes are damaged

repair

demyelinated areas fill with ______ _________

fibrous astrocytes

what ocurs with demyelination that forms glial scars or plaques

gliosis

Radiologically Isolated syndrome (RIS)

MRI findings suggestive of MS without typical clinical manifestations; 30-50% develop first sx in 10 yrs

Clinically isolated syndrome (CIS)

first clinical demyelinating event suggestive of MS; sx typically last ≥ 24 hr and are not better explained by fever/infxn/other

Relapsing-remitting multiple sclerosis (RRMS)

relapses followed by periods of recovery; no progressive worsening between relapses; may transition to SPMS

Secondary progressive multiple sclerosis (SPMS)

begins with a relapsing course and transitions to progressive accumulation of disability

Primary Progressive MS (PPMS)

progressive accumulation of disability from disease onset

active meaning

evidence of new inflammatory disease activity

not active meaning

no identified inflammatory disease activity during the specified time period

with progression meaning

gradual accumulation of disability over time

without progression meaning

non documented gradual worsening over the specified time period

smoldering MS

chronic compartmentalized inflammation and neurodegeneration occurring outside of acute relapses

DIS locations

periventricular, cortical/juxtacortical, infratentorial, spinal cord, optic nerve

is DIT mandatory for dx

no, not when other evidence supports dx

biomarkers

OCBs can support DIT, intrathecal k-FLC as an alternative to CSF restricted oligoclonal bands

MRI markers

central vein sign, paramagnetic rim lesions

corticosteroids in MS management

manage acute relapses; short term use, side effects limit long term use

disease modifying therapies in MS management

reduce frequency/severity of relapses, slows progression

symptomatic agents in MS management

manage spasticity, increase walking speed, treat fatigue

EDSS 0-3

minimal to moderate disability

EDSS 4.0

fully ambulatory despite severe disability

EDSS 5-9

loss of ambulation, full daily activities impaired

psuedo exacerbation

temporary worsening of sx from heat, infxn, exertion

older age linked to faster or slower disability progression

faster

younger age at onset linked to...

longer duration to disability but younger age with severe disability

males or females associated with higher risk of rapid disability

males

what 3 comorbid conditions worsen long term prognosis

cardiovascular, psychiatric, smoking

what lesion location causes higher risk of severe disability

spinal cord

what biomarkers at dx are associated with worse outcomes

CSF oligoclonal bands

common MS body function/structure impairments

weakness, spasticity, sensory loss, visual disturbances, ataxia, tremor, impaired coordination, fatigue, fatiguability, bowel/bladder, mood changes, cognition

common MS activity limitations

reduced gait speed, reduced walking endurance, impaired balance, stair and transfer difficulty, DT difficulty, ADL inefficiency

possible contributors to foot drag during swing

ankle DF or hip flexor weakness/fatigability, spasticity or poor motor control

possible contributor to unsteady gait

sensory, visual, vestibular, or cerebellar contribution

PT primary focus during early/mild MS

prevent secondary decline, restore and maintain function

PT primary focus during middle/moderate MS

maintain mobility; combine restorative and compensatory care

PT primary focus during late/advanced MS

prevent complications; preserve comfort, participation, caregiver safety

you cannot repair the CNS damage through therapy but you CAN...

prevent the indirect impairments from disuse and sedentary lifestyle