Multiple Sclerosis Flashcards
What is MS
chronic and debilitating disease that results from demyelination of the CNS
onset between 20-40 y/o
sclerotic plaques form throughout brain and spinal cord
charcots triad: intention tremor, scanning speech and nystagmus
presentations of symptoms not consistent from one pt. to another
pathophysiology
most accepted theory is that some environmental trigger, virus, causes a delayed autoimmune attach in genetically susceptible people
what occurs with MS
patches of demyelination occurs in the white matter of brain and SC-> destruction of oligodendrocytes= myelin producers
inflammation accompanies that destruction of myelin shealth and can lead to axon damage and plaque formation
plaque replaced by scar tissue produced by GLIAL CELLS
what are glial cells
what produces the plaque on scar tissue in MS and causes degeneration of trapped axons
what areas of nervous system are most likely affected
optic nerve
periventricular white matter
corticospinal tracts
posterior columns
cerebellar penducles
clinical manifestations
sensory changes
pain
visual disturbances
motor dysfunction-impairment
ambulation
speech and swallowing dysfunction
cognitive and affective changes
autunomic changes
Sensory Changes
paresthesia-pins and needles sensation
typically first signs
Visual changes
optic Neuritis: blurring, loss of vision, pain on eye movement
Scotoma: blind spot
NYstagmus: rapid, alternating oscillations of the eyes
internuclear ophthalmoplegia: lateral gaze palsy
diplopia: double vision
Pain
trigeminal Neuralgia: short attacks of severe facial pain
Lhermitte’s Sign: sensation like electric shock running down the spine and into limbs, produced by flexing nek
hyperpathia: hypersensitivity to light touch or pressure stimulus
chronic neuropathic pain-burning pain
UMN Weakness and fatigue
Weakness/paresis- mild to total
fatigue-persistent, loss of energy, limited tolerance to ex
spasticity
UMN
occurs 80%
varies from mild to severe
may include: Conus, spontaneous, positive Babinski
Balance and Coordination
ataxia-uncoordinated movements
dysmetria: inability to judge distance or ROM
dysdiadochkineisa: inability to alt. movements rapidily
dyssynergia: impaired ability to perform movements in a complex movement or associate together
Postural tremor: shaking, back and forth oscillatory movements
Intention Tremor: vary from slight to severe during voluntary movements
Ambulation
weakness/paresis fatigue spasticity impaired sensastion visual problems ataxia
speech and swallowing
dysarthria: slurred or poorly articulated speech
* *slow rate, low volume and unnatural emphasis
dysphonia: changes in vocal quality
* hasness, hoarseness, breathiness, hypernasal sounds
Dysphagia: difficulty in swallowing
Cognitive and affective Change
mild to mod. impairments
depression
affective changes
**pseudobulbar affect: sudden loss of emotional control=emotional lability
**euphoria: exaggerated feeling of well being
- cognitive inflexible-caused by lesions in frontal lobe=unable to change or adapt
- -loss of ability of judgement and reasoning
Fatigue
most frequently reported symptom
persistent and loss of energy
limited tolerance to ex
worsened by heat
can affect ability to complete ADL’s
autonomic changes
Urinary and bowel issues
cardio dysautonomia
sexual dysfunction
Motor Features
clumsiness in reaching and over shooting target
postural tremor of extremity or trunk in sitting or standing
scanning speech is slow with long pauses and lacks fluidity
increased risk of aspiration
gait is characterized by poor balance and lurching
Relapsing-remitting Course
periods of exacerbations and remissions
occur when sympotms worsen acutely and thenr emit or recover with time of symptom stability
intervals btw. exacerbation may initially be a year or more at beginning of the disease
-intervals may shorten as the disease progresses
Primary Progressive
relentless progression without any relapses
secondary progressive
begins w/ relapse and remissions but then becomes progressive with only occasional relapses and minor remissions
progressive relapsing
progressive from onset but has clear acute exacerbations with and without full recovery
benign
describes clinical course in which symptoms progress very little over the span of the persons life
malignant
progressing symptoms that quickly result in disability and death
diagnosis based on
clinical evidence of multiple lesions in CNS white matter
distinct time intervals
occurence in indiviuals btw. ages of 10 and 50 yrs old
CSF examined for higher amounts of gamma globulin and myelin protein
4 injectable drugs
reduce frequency of attacks as well as disease progression
- Copaxone- synthetic compound made of amino acids– reduce inflammation at lesions sites by stimulating T cells to increase anti inflammatory agents
- interferons
- avonex
- betaseron
- rebif
6 PT goals
- minimize progression
- maintain an optimum level of functional independence
- prevent or decrease secondary complications
- maintain respiratory function
- conserve energy and maintain energy levels
- educat pt. and family
sensory deficits
diminished sensation=retraining via stimulation tech
proprioceptive loss
blurred vision
double vision
skin care prevention
skin should always be kept clean
good diet and fluids
inspect skin daily
clothing should be breathable and comfortable
provide regular skin relief
-move every 2 hours lying and 15 minuntes sitting
management of pain
chronically weakened muscles
pain due to malalignment
stabbing pain from L hermitte’s sign-relieved with soft collar to limit neck flexion
painful dysesthesias
Exercise Training
schedule sessions on alternate days and times
sub max ex around 60-75% peak HR or 50-60% VO2 max
alternate work btw. UE and LE
balance ex with adequate rest periods
Slow progression
exercise to point of fatigue is contracindicated
monitor effects of fatigue
manage core body temp and prevent over heating
