PD Flashcards
1 risk factor for PD
age
etiology of PD
degernation of dopaminergic cells in substantial compacta
-oxidative stress
cell inability to remove toxins - free radicals - aptoptosis
programmed cell death
inc level of excitatory AA (glutamate)–> cell death
cause of PD
genetic: 15-25% people w/ PD have fam member w/ it
* tendentcy for onset to occur around same year, suggest enviro exposure
enviro: pesticides, water well, wood pulp mill, rural areas, agent orangeinverse relationship w/ nicotine
PD and basal ganglia
decreased dopamine receptors
decrease in dopamine, serotonin, norepinerphrine
areas of brain affected by PD (loops)
motor circuit
asccociative loop
limbic loop
PD dx
clinical (by reported symptoms)
dopamine transporter scan - for diff dx for atypical
10 common first signs of PD
resting tremor rigidity bradykinesia stoop posture hypokinesia sleep disturbances constipation loss of smell micrographia dizziness
tremor and PD
resting, keep hand in flexion to control
may involve UE or LE or both, type starts on one side
may increase when exited or anxious
rigidity and PD
primary impairment of PD
common complaint is of stiffness
severity directly related to dopamine loss
rigidity in trunk leads to decreased axial rotation
lead pipe rigidity
uniform hypertonicity throughout passive motion
cog wheel rigidity
increased resistance to passive stretch that gives way in small increments
clasp knife repsonse
characterized by a sudden decrease in resistance to passive movement
dystonia and PD
abnormal sustained muscle contraction causing twisting or turning around one or mult joints
dysfunction at basal ganglia causing excessive motor output
-early symptom or complication of tx
dyskinesia and PD
involuntary movements
looks like writhing, tics, chorea
occurs as result of med - excess dopa from replacement therapy
proprioception and PD
should be intact
PD mismatch b/n intended and actual output
believe they re moving normally when they are in fact not
true for motor and speech
**problem is central not GTO
PD gait devations
dec stride length dec speed lack of heel strike decreased or absent arm swing decreased trunk rotation stooped posture festination
PD and freezing cause
change in enviro cognition-dual task turning target initiating movement
PD freezing and gait
narrow BOS
lack of WS
PD cog S/s - risk
older age at onset
longer duration of s/s
rigidity
hallucinations or psychosis
PD - dementia w/ levy bodies
15-30% cases of cog impair
lewy body in substantia nigra
protein aggregate surrounded by fibrils (10nm)
PD dementia
no lewy body, better outcome
more responsive to DRT
ppl w/ greater mitral neuronal loss
prevalence related to age
PD decreased executive fx
poor mental flexibility or set shifting poor dual tasking decreased attention poor visual spatial orientation impaired memory word finding deficits
PD: hoehn and yahr stage: 1
unilateral movement
minimal to no functional disability
PD: hoehn and yahr stage: 2
bilateral or midline involvement
w/out impairment of balance
PD: hoehn and yahr stage: 3
bilateral disease
mild-mod disability w/ impaired postural reflex
physically indep
PD: hoehn and yahr stage: 4
severely disabling disease
still able to walk and stand unassisted
PD: hoehn and yahr stage:
confined to bed or W/c unless aided
PD poor prognosis if presents w/
older age at dx early cog deficits associated co morbidities dec repose to dopamine replacement greater baseline impairment dx of MSA or PSP rigidity and bradykinesia
PD improved prognosis
right sided tremor is first symptoms
progressive supra nuclear palsy
atypical parkinsons
-loss neurons and gliosis –> neurofibrillary tangles in cerebral cortex, decreased blood flow (frontal lobe), decreased oxygen utilization in central structures
typical onset after 60, M>W severe disability 3-5 years after onset
progressive supranuclear palsy most common first complaint
unsteadiness of gait w/ unexplained fallings
how is PSP diff from PD
PSP progresses more rapidly, severe speech and swallowing, minimal repose to PD meds, may retropulse
lack of vertical eye movements and saccades, eventual loss of convergence, small pupil, saccadic smooth persuit
how is PSP like PD
age at onset bradykinesia tremor rigid apathy cog impair
multi systems atrophy includes
striatonigral degeneration
shy drager syndrome
oliviopontocerebellar degen
multi systems atrophy categories
MSA -P: mild tremor, illness begins w/ hypotension
MSA-C: cerebellar ataxia, dysphonia w/ stridor present
*wheter they are predominately parkinsonism or cerebellar ataxia
either: autonomic dysfunction: postural hypotension, bladder, dysfunction, fecal incontinence
MSA distinguishable from PD by
symmetry of signs
early presence of autonomic dysfunction
minimal tremor
lack of response and dopamine
atypical or parkinson’s plus diff dx symptoms
eye movements, PSP lack of vertical, or eye tremor tandem balance, bicycle, potential MSA response to meds speed of progression lack of progress sever hypotension w/ postural changes
PD med tx
- med
- deep brain stim
- PT
levadopa
not started till later
MAO-b inhibitor
neuroprotective benefits
may prevent breakdown of existing DA
dopamine agonist
increase update of existing dopa
side effects include compulsive behavior and hallucinations- alert MD, needs to be altered
dopamine replacement therapy
1/2 life = 4 hours, protein interferes w/ binding/absorption
side effect: orthostatic hypotension
complications: wearing off, dyskinesia, dystonia
*motor complications occur in 50% w/ PD after 5 years on levadopa
DRT on off effect
on: meds working
off: meds not working
15-20% of its have severe motor fluctuations leading alternating periods of dyskinesia and immobility
COMT inhibitor
slows breakdown of levadopa
heals w/ wearing off
Amantadie
antiviral for dyskinesia (which is result of meds)
PD consideration w/ meds and exercise
most commonly prescribed drugs are hypotensive agents
aberrant learning and role of medications
if you learn a motor program wrong the first time, it is a lot harder to learn the correct one w/ practice
w/out dopa, PD learn wrong first time compared to on dopa
DBS
deep brain stim
sx implant of pacemaker
send electrical impulse to stim brain
implanted globus pallidus internen or subthlamic nuclei
best candidates of DBS
good response to levodopa but have severe motor fluctuations that can’t be controlled w/ meds alone
interlate to meds
<70 yrs
DBS contras
cog/psych problems
atypical PD, speech or swallowing progblems
frequent falls
decreased motor performance when on levadopa
PD PT indications
prevention decreased fx mobility including gait dev pain (shoulder: posture. back: rigid) posture balance
falls occur in ___% of PWPD
68%
exercise for neuroprotection
increase release of dopamine
increased number of dopamine receptors, more efficient w/ exercise
**exercise must start early
Exercise is med
improve cog fx prevent depression improve sleep quality decrease constipation decrease fatigue improve motor performance improve drug efficiency optimize dopaminergic system
montreal cog assessment
MoCA
>/= 26/30 normal
use score to justify ST referal
dystonia
abnormal sustained muscle contraction
document body part, trigger, how it interferes /w movement
retropulsion
tendency to fall backwards
dyskinesia
excessive movements, wristhing
disorder caused by meds
doc where, how if interferes w/ function
shoulder pain and PD
common
related to postural changes
eval thoracic mobility, scapular mobility, SHR
which measures of physical function and motor impairment best predict quality of life in PD?
freezing of gait
6MWT
freezing of gait questionnaire
16 items eval
- gait of daily living
- freq/severity of FOG
- freq and festinating gait and rln to falls
- frequency and severity of alls
best question to ask if you only have time for one questions (PD)
“do you feel your feet get glued to the floor while walking, making a turn or when trying to initiate walking?”
reliable for ID freezers
ways to provoke freexing
add turns dual task wake through doorway/narrow space walk over lines in ground or change in floor type add urgency
gait analysis - PD
trunk rotation step length arm swing freezing festination shuffling lack of WS
10 m walk test
0.88m/s correctly predicted 70% of pts as community walkers
MDC value (95%) comfortable gate speed = .18m/s fast gate speed = 0.25 ms/
FGA review
22/30 fall risk
15/30 fallers in PD pts
score 0-3, severe imp to normal amb
mini best review
14 dynamic balance assessments
0 severe, 1 mod, 2 normal
<20/28 fall risk
if L and R, lower score used for total score
4 square step
fall risk for PD
>9.68 seconds
phases of PD intervention
- preclinical - neuroprotection
- early/mod - neurorepair
- late - adaption
evidence based practice for PD
treatmill training
high intensity resistance training
cycle
aerobic exercise
treadmill training and PD
increased gait speed, stride length after 1 session
feasible, safe, improve gait speed, stride length
improve QOL, UPDRS, long term carryover
FE
forced exercise for PD
global improvements w/ high intensity aerobic exe cerise on tandem bike
improve bimanual coordination 4 weeks
decreased tremor, rigidity, bradykineasia
high intensity resistance training PD
safe, muscle force production, pain, serum creatine kinase
hypertrophy, strength, improved speed w/ stair descent, improved 6MWT
decreased brady, improved QOL
improved rise from chair for CRE
high intensity resistance training: focus on
postural extension hip ext, ab knee ext gastric/soleus trunk ext
