Lecture 7: Parkinsons Evaluation Flashcards
PD
Progressive disorder of the cns
has both motor and non motor symptoms
motor symptoms: cardinal features - these are what makes it unique
* bradykinesia
* tremor
* rigidity
* postural instability
onset is insidious w/ slow rate of progression
disruptions in daily functions, roles, and activities
what is the scale for pd
Hoehn-Yahr classidication
* stage 1 = minimal
* stage 5 = severre
what si 1 on the modified hoen yahr scale?
unilater involvement only
typically not diagnosed because dr. will just say they need sleep/too much stress causing that little tremor
what is 1.5 on modified hoehn yahr
unilateral and axial inolvement
* but not postural
what is a 2.0 on the modified hoen and yahr
bilateral W/O impairment of balance
* they can feel balance problems coming but dont actually have them yet.
what is a 2.5 on the modified hoen and yahr
mild bilater disease w/ recovery on pull test - so they dont fail it
what is a 3.0 on the modified hoehn yahr
mild to moderate bilaterl disease; some postural instability; physically indepdent
what is a 4.0 on the modified hoen yahr
severe disability; atill able to walk/stand unassited - will be very ugly gait
* but can use an assited device? ask
what is a 5.0 on modified hoehn yahr?
wc bound or bedridden unless aided
what is the pull test?
you pull them backwards and they catch themsevlves - should pull enough where they must take a step correct
* you catch them if they fall
hoen yahr unmodified
movement disorder society-sponsored revision of the unifed parkinsons disease rating scale
* modification renamed
* goals of revision: improve ability to detetct slower and smaller changes in mildly disabiled pts and increase focus on nonmotor symptoms
* 4-part structure with reworking of questions and additional 6 items
* total 48
* four point scale (0, no, or 1, yes, in the original scale)
* 0 normal or no problems; 1, minimal problems, 2, mild problems, 3, moderate problems; and 4, sevre problems
* part 1 = non-motor aspects of experiences of daily living
* 2 = motor experiences of daily living
* 3 = motor examinination
* 4 = renamed motor complications
* 30 mins to adminster
* parts 1 and 2 designed to be self adminstered by pt
detect smaller changes - pt is saying they’ve having small changes but other tests fail to catch these small things
this questionaire is supposed to be the subjective portion of how pd affects their lives
motor and non-motor symptoms in pd progress together - duh
non motor symptoms w/ pd come before or after motor?
they come first (up to 10 years earlier!)
orthostatic hypotension - may not be super severe initially
lack of sleep/sense of smell common
early symptoms - before motor - before disease really becomes apparent
apthy = lack of feeling or emotion
stuff about pd
* second most common neurodegenerative disorder
* estimated 1 in a millin americans
* 7 to 10 million people world wide
* incidence increases 5-10x in 60s to 90s
Prevelence
* under 1% of people aged 45 to 54
* 4% of men and 2% of women aged 85 and older
- prevelence expected to more than double by 2040
- average age of onset=60
- 4% to 10% of patients diagnosed before age 50
- early onset PD/Young onset PD: between 21 and 50
- juvenile onset <21
- men 1.2-1.5 times more likely than women
not asking these #’s
clinical course PD
* progressive
* Long preclinical/prodromal period estimed 5-25 years
* variability in the rate of pression
* young age or tremor predominant typically more benign progression - so these are good things
* postural instability and gait distruabnces more pronouced deterioration with more rapid diseqse progression - so these are bad things
* neurobehavioral disturbances and dementia common - end stage - makes you mean
* common causes of death-cardiovascular disease and pneumonia
if they respond to levadopa they have parkinsons
anything that can impact the bg can cause parkinsons symptoms
dont memorize
Rigidity - comes w/ pd - velocity indpendent and doesnt matter the direction
* clinical hallmark sign of pd
* increased resistance to passive motoin - quiz - not active (because bsically the agonst and antagonst are both firing making it hard to move extrememity)
* fairly constant regardless of task, amplitude, or speed of movement
* onset assymetrical, espeically in early stages - so think one arm will move more than the other
* tyically impcts proximal muscles first-shoulders and neck-cprogresses to muscles of face/extremitites)
* decreases ability to move easily
* active movement, mental concentration, or emotional stress may all increase rigiditty
* prolonged rigidity results in decreased rom and serious, secondary cimplications of contracture and postural deformity
* direct impact on increasing resting E (- they have to use more e at rest) expenditure and fatigue levels
* can vary during day, point in medication cycle, and w/ stress
dont use modified ashworth - use PROM
bradykinesia - slowness of movement
* cardinal feature pd
* weakness, tremor, and rigidity may contribute to bradykinesia but do not fully explain it
* insufficient recruitment of muscle force during initiation of movement
* underscale movement commands internally generated movements
* one of the most disabling symptoms of pd, with prolonged movement and reaction times resulting in increased time on task and dependence in daily activities
* bradyphrenia-slowness of thought can contribute to brandykinesia - quiz
* hypokinesia-decrease in amlpitude of movement
* later stages, movements become arrhythmic w/ frequent start hesitations and arrrests (akinesia)
we treat the bradykinesia the most
* w/ this big movements
how we test bradykinesia
can take a stop watch and time how long it takes for them to start a motion after being told to start
* can do tug etc…
* rapid alternating movements timed (dysdiadochokinesia)
when someone w/ pd walks that trunk motion goes away = hypokinesia
micrographia - handwriting gets smaller as they write
tremor
* cardinal feature of pd
* involventary shaking or oscillating movement of part or parts of body resulting from contractions of opposing muscles
* early stages of the disease = 70% of pts
* tremor = less severe when pt is relaxed
* aggreavted by stress
* later stages tremors become severre
* fluctuations in frequency and intensity are common
explain a resting tremor
pt at rest suppressed briefly by voluntary movement, and disappears w/ sleep
* typically if they do movement it goes awat
* this is just a tremor when theyre hanging out
postural tremor
tremor of head and trunnk seen when muscles are used to maintain an upright posture against gravity
* gets worse when they have to use those muscles
action tremor
(intention of kinedtic) tremor that continues w/ movement, can occur in pts w/ advanced disease
* more in advanced stages
if this is their first sign thats bad
lots of different things impact this
* some can be improved
in pd, we really need to know what stage of the disease were in
* early = thinking more recovery
* late = compensation/comfort
postrusl deformity
progressive
weakness of antigravity m (spinal extensors) contributes to a flexed, stooped posture with increased flexion of the neck, trunk, hips, and knees
change in center of alignment position, positioning individual at forward limits of stability
LE contracture
* hip and knee flexors
* hip rotators and adductors
* pf’s
spine
* dorsal spine nad neck flexors
ue contracture;
* shoulder adductors and ir
* elbow flexors
deverive the above by knowing they’re in a forward hunched posture
fucntion becomes progressively more limited by msk constraints
standing, typically flexed, stooped posture (kyphosis w/ forward hd) w/ com placed forward within limits of stability
* so some of these body mechanical deviations can lead to worse postural instability - not jsut weak m
supine flexed posture w/ forward hd still evident (shadow pillow posture)
LE contracture more evident than UE
* more contractures = less function
shadow pillow contracture
pts w/ pd fall a lot
* they have balance problems
hip fx common
in acute care they wont want them to get up if they’re a fall risk - however we need them moving
medication management is very importnt w/ pd - needs a very specific time - and multiple doses a day
first fall = more likely to fall again
scared of falling = increased risk of falls
do outcome measures to see if they’re at risk for falls
protective responses 6,8,10
* can test these as well in adults
know: tinneti is not sensitive to sensing change in gait for pts
easy to ceiling on berg
* dont do this unless u actually see balance problems or they’re going to score 100
not going to have us dilinate between primary and secondary impairments
* becuase some of the things on our secondary impairment list can also be primary
m performance w/ pd - lots of reason - because muscles don’t fire the same way, its asynchronous (meaning some muscles myofibrils contract and other dont) - timing of actually turning on the muscles is altered
* reduction in strength
* torque production decreased at all speeds
* activity limitations and muscle weakness
* changes in strength may be dopamine related
* “on” state demonstrate increases in strength
* EMG motor unit recruitment delayed w/ under recruitment of muscles
* once initiated contraction characyrrized by multiple bursts and asynchronizayion-pauses and inabiliy to smoothlu increase firing rate as contraction continues
* compounded during production of complex movements
* disuse weakness evolves from inactivity and increases movement difficulties - keep pts moving w/ pd
more worried about functional than mmt
gait w/ pd
* 13-33% of pts present w/ postural instsbility and gait disturbanced
* gait disturbnces common in late-onset or advanced
* reduction in arm swing w/ asymmetry
* some pts can only stop when they run into something
if you see the word festinating giat pattern pick pd as the answer
progressive increase in speed w/ shortening of stride- multiple short steps to catch up w/ com to avoid falling, and may eventually break into run or trot
festinating of gait
cannot stop themselves
* can get so bad that they cant stop unless they run into something
a forward festinating gait
anteropulsive
a backwards festinating of gait
retropulsive
* less common
need multiple steps to change directions
decreased step length
freezing of gait
when you tell them to walk faster they increasenthe cadence and decrease step length
* a normal person increases stride length
so measure how long it takes from when you say go and they actually start walking
* if you get any time its too long
variability = can be path deviations
* assymerical in pd - typically perfurred to one side
* i think this is pirimairly due to rigidity being assymetrical
they might have a hard time stopping when you say stop. count the # of steps they take after saying to stop (festinating of gait)
freezing of gait is vairable so its hard to measure
* typically happens when walking through something/some kind of distraction
incressed double limb support
* anyone w/ balance difficulties spends more time on both legs
fear of falling = give them a dual task in walking and this can decrese the fer of falling and they’ll go faster - w/ pd
* only works in early stages
complex environments = harder time walking
becomes a social problem because people notice
* will make them want to isolate
fatigue -different than just feeling tired “entire body slows down” - cogntive fatigue can be frusturating - takes more energy all thre time because of the rigidity
* one of the most common symptoms
* difficulty in sustaining activity and increasing weakness and lethargy as day progresses
* activitiws start strong but decrease in strength and amplitude as activity progresses
* performance decreases dramatically w/ physical effort or stress
* rest or sleep may restore mobility
* L-dopa therapy-less fatigued
* long standing disease and drug therapy, fatigue typically reappears
* increased sense of effort associated w/ movement
helps classify how fatigued someone is
Sensory symptoms
* do not suffer from primary sensory loss
* up to 50% experience paresthesias and pain
* Pain may be due to diseases effect on central nociception - this is positionaly and intermittent
* symptoms typically intermittrnt and vary in intensity and location
* pain more intense in off state
* postual stress syndrome secondary to faulty posture, ligamentous strain, lack of movement, and muscle rigiidty
most pts get dysphagia by end stage (difficulty swallowing)
* can come on at any stage
problem is aspiration
* can even do this on own spit and cause pneumonia
* could make them just not want to eat
sialorrhea
excessive drooling as result of increased saliva production and decreased spontaneous swallowing
* can make them apsirate on nothing but spit
can also make them not want to go out in public
are very monotoned
* uncontrolled = can talk to fast or slow
* basiclly sounds like a whisper - we tell them to yell
* we work on this by improving breath support / head support / posture - makes it easier to talk
* they think they’re talking loud
psychosis = hallucinations
hallucinations impacted by medications they’re on
neurochemical imbalances
psychosocial problems
multifacotral
hypomimia
reduction in facial expressiveness, can give the appearance of depression
anyone who has all the stuff mentioned above would give a noraml person anxiety
agroaphobia - not leaving house at all
autonomic dysfunction
go from hot to cold etc…
orthostatic hypotension
* common in middle to late pd
* sharp drop in bp w/ positional changes
* typical symptsoms: lightheadedness or dizziness, pallor, diaphoresis, weakness, trembling, nausea, difficulty thinking, or syncope
* risk for lob, falls, and injury
* medications levodopa/carbidopa, bromocriptine
* drop in systolic bp of 20 mmhg or drop of 10mmhg in diastolic bp and a 10-20% increse in pulse rate is diagnostic
to test:
* supine for 2-3mins - resting hr and Bp are taken
* supine to sitting wait at least 1 minute, bo and hr are taken
* pt stable after at least 3 mins -move to standing
* stanf bp and hr again taken after at least 1 min and repeated between 3 to 5 mins
* bp that continues to drop after at least 1 min of standing = problematic and evidence of advanced disease
cardiac response to pd
* early and progressive sympathetic
denervation of the heart occurs in the majority of pts
* results in diminished heart function-may be contributory factor in fatigue
* advanced pd exhibit altered hr and bp during ex w/ decreased ex efficiency
* mild to moderate do not appear to demonstrate significantly different exercise capacity (maximal hr, maximal o2 consumption) when compared to age-matched controls
often due to lack of ambulation
* m pump gets rid of it
rem sleep beahvior disorder = lack of sleep paralysis so move all over the place at night
* wake up not rested because they were moving half the night
<15% of calories should be from protein
* high protein can block the effect of L-dopa
* should be high calorie diet low in protein
