Parkinson's Disease Flashcards
Pathophysiology
Pars compacta section of substantia nigra recieves overall loss of dopamine –> increased activity of indirect pathway –> increased inhibition of movement
5 Classic features of parkinson’s
- Rest tremor (toe rolling)
- Rigidity
- Bradykinesia
- Loss of postural stability (test with pull test)
- Flexed posture
Variable features of parkinson’s
- Freezing of gait (address by aiding in weight shift)
- Dystonia
- Micrographia (small amplitude of writing)
- Orthostasis (side effect of sinemet)
- “bradycrania”
- Dementia (later stages)
- depression
4 implications of flexed posture
- loss of trunk rotation
- loss of pelvic rotation
- smaller step lengths
- influence ability to shift weight
Stages and Descriptions of Parkinson’s Disease (Hoehn and Yahr)
Stage 1: unilateral (UL tremor, foot drop/drag)
Stage 2: bilateral
Stage 3: mild-mod disease, postural instability, physically independent (+ pull test)
Stage 4: req assistance for standing and walking
Stage 5: confined to bed or w/c
Circuitry through the Basal Ganglia
Direct (facilitation of movement) and Indirect (inhibition of mvt) pathways through putamen and globus pallidus –> substantia nigra –> thalamus –> back to cortex
*health movement = balancing act between direct and indirect
4 Circuitry loops through Basal Ganglia
- Sensorimotor Loop - select appropriate motor response, inhibit inappropriate response
- Occulomotor loop - ocular deviations in BG disorders
- Association loops- issues crossing info across cortex; role in stimulus response tasks and implicit memory
- Limbic Loops- filtering appropriate emotional responses
Lewy Bodies
abnormal collection of alpha-synuclein proteins is a hallmark of Parkinson’s; as the disease progresses, more and more lewy bodies and lewy neurites move through brainstem and into cortex (substantia nigra is one the the early levels of the brainstem affected)
Differential Diagnoses of Parkinson’s
- Normal Pressure Hydrocephalus
2. Parkinsonism
Cause of PD, age of onset
no known cause yet, small genetic component (earlier onset)
normal age of onset is after 50
Normal Pressure Hydrocephalus: similarities and differences in parkinson’s disease
Similarity: presentation of shuffled gait with low postural stability
Difference: NPH presents with gait symptoms first, manifested later in PD
Similarity: enlarged ventricles on MRI
Difference: with spinal tap, increased pressure in Ventricular System with NPH, NOT with PD (no inc pressure)
NPH treatment: shunt via catheter in spinal canal; resolves gait presentation
Parkinsonism: Cause
Drug induced: psychiatric medications (antipsychotic meds)
Parkinsonism: Symptoms
- Progressive supranuclear palsy (presentation of eye dysfunction; usually upgaze first)
- Multisystem atrophy (umbrella term for degeneration in 3 different tracts- can get symptoms from any)
Progressive Supranuclear Palsy; pathogenesis and prognosis
Roll of superior colliculi is integration of visual information. Dysfunction in SC –> limitation in occulomotor function. Specifically affects CN IV (sits between SC and IC) –> innervation for superior oblique oculomotor mucle –> upgaze usually affected first
*prognosis = 4 years post diagnosis
Multisystem Atrophy; types, tracts affected, and presentations
- Olivo Cerebellar Atrophy: cerebellar tracts, intention tremor
- Striatoniagral Degeneration: gait dysfunctions, tremors, slowed movements
- Shy Drager Syndromes: ANS dysfunction; severe hypotenstion (prognosis = 5yrs)
Medications used in PD
- Levadopa/Carbidopa (Sinement)- for bradykinesia
- Dopamine Agonists - increase dopamine in synapse
- Anticholonergics - block ACH, aid in tremor modification
- Neuroprotective - slow degenerative process
- Amantadine (Symmetrel)- dopamine agonist
- COMT inhibitors
- Tolcapone (Tasmar)
Levadopa/Carbidopa (Sinemet)
- purpose
- biological effect
- side effects
- Administration
purpose: helps in bradykinesia, if too much- aberrant movements
Biological effect: prevent breakdown of levodopa in the gut
Side effects:
- postural hypotension
- dyskinesia
- psychosis
Administration: only in small doses; loses effectiveness over time; on/off periods during the day
Dopamine Agonists
- Ropinirole (Requip)
- Pramipexole (Mirapex)
- Bromocriptine (Parsidol)
- Pergolide (Permax)
??5. Amantadine (symmetrel)?
Anticholonergics; meds and side effects
- Benztropine (Cogentin)
- Ethopropazine (Parsidol)
- Triheyphenidly (Artane)
Side effects: confusion, drowsiness, dry mouth, nausea/vomitting, constipation
Neuroprotective drugs
- rasagiline (Azilect)
2. Selegiline (Eldypryl, Deprenyl)
Brain Stimulation and PD
Treatment method performed at end point of medications
Very effective for bradykinesia
introduces electrical current into subthalamic nucleus to change the bias of direct/indirect system
MDS-UPDRS
Body structure body function scale, rates all the signs and symptoms of parkinson’s
PDQ-39
Participation scale for PD, rates the QOL on 8 subscores: mobility ADLs emotions stigma social support cognition communication bosy discomfort
Direct v Indirect effects of PD
Direct = nervous system
Indirect = non-nervous system (MSK, cardiopulm, GI, urogenital, psychological)
* both combine to form impairments and disabilities in PD
Flow of movement
Initial conditions –> preparation –> initiation –> execution –> termination –> outcome
*breakdown can occur at any 1 of these stages
Early Stages of PD: common impairments and functional limitations
- UL tremor
- mild rigidity
- mild gait hypokinesia
- micrographia
- reduced speech volume
Middle stages of PD: common impairments and functional limitations
- some functional limitations
- speech impairments
- BL bradykinesia
- Rigidity
- Gait impairments
- May require assistance at end of this stage
Later stages of PD: common impairments and functional limitations
- severly impaired, disabled, swallowing and pulmonary function compromised
- dependent in all mobility and ADLs
- bladder dysfunction, incontinence
Early stages of PD: intervention- restorative/preventative strategies
ACSM guidelines for aerobic, strength training, flexibility, and balance training in older adults
Early stages of PD: intervnetion- compensatory strategies
education about the disease, support group
Middle stages of PD: intervention- restorative/preventative strategies
- ACSM guidelines
- Monitor for depression, psychosis
- Badykinesia- task practice, vary speed demands
- Postural control/balance - stepping strategies in backwards and turning
- gait training- hypometric and bradykinetic, weight shifts, feezing, DUAL TASK practice
- Motor planning- task practice
- Freezing- address mvt transitions and perception of environment
- simultaneous v sequential movements
Middle stages of PD: intervnetion- compensatory strategies
- mvt strategies for akinesia
- environmental analysis: restructuring visual/auditory/manual cueing
- Provision of ADs
- Education to caregivers, functional training
Late stages of PD: intervention-preventative strategies
- pulmonary hygeine
- skin care
- education of caregivers (prevent secondary complications)
Later stages of PD: intervention- Compensatory strategies
- education of caregivers (lifting, transfers, bed mobility)
ACSM Activity recommendations for older adults: Aerobics
Virgorous intensity: 20min 3days/wk
Mod intensity: 30min 5 days/wk
ACSM Activity recommendations for older adults: strengthening
8-10 exercises involving major muscle groups- 10-15 reps each, 2days/wk
ACSM Activity recommendations for older adults: Flexibility
8-10 exercises involving major muscle groups- 2-4 reps each, holding 15-30s, minimum 2-3days/wk
*ideally 5-7days/wk
ACSM Activity recommendations for older adults: Balance
exercises to improve balance
Curtis and Bassile: Individuals with PD: Physical Activity Perormance and QOL in Individuals with Early Stage PD and their partners
Found that not many pts with early stage PD are getting the ACSM recommended activity.
Outcomes used: CHAMPS physical activities questionnaire for older adults, SF-36, Social and medical information
Dibble et al (2006): High Intensity Eccentric Resistance Training in PD
Found that a high intensity, eccentric training group had improvements in
1. quad muscle volume on MRI
2. increased 6MWT, stair ascent/descent time
Conclusion: we should work PD population harder and include eccentric exercise
Fisher et al (2008): High Intensity TDM training in PD
found that a high intensity exercise group had:
- increase in gait speed, step length, hip/ankle joint excursion
- improved weight distribution in STS
- lengthened cortical silent period on TMS
Horack et al (2005)
confirmed presence of bakwards instability as characteristic of PD
PD pts had much smaller sway envelope
Potential causes: neural or postural issues
Hackney and Earhart (2008): Backwards walking in PD
PD pt have impaired foward and backwards walking, but differences between PD and controls is higher in BW, suggesting that BW is impacted earlier in the disease process
Curtis & Bassile: Effects of exercise on balance, movement speed and functional mobility in individuals with parinson’s disease
Looked at PLM test (postural phase, locomotion phase, and manual phase): test looks at ability to perform phases simultaneously
Conclusion: PD pts had lower ratio of overlap= simultaneity of movement is affected
