Parkinson's disease Flashcards
define parkinsons
Parkinsonism: a syndrome manifested by part or all of symptoms of resting tremor, bradykinesia, and rigidity (with resulting postural instability)
Parkinson’s disease is a specific chronic progressive neurodegenerative disease with features of Parkinsonism
Key factor: loss of dopamine-producing cells in basal ganglia
First described by James Parkinson in 1817
No cure
aetiology
Characteristic feature: degeneration of dopamine-producing cells in substantia nigra pars compacta of the basal ganglia
Unknown cause
Environmental factors + genetic predisposition
Cellular mechanisms: Oxidative stress, premature apoptosis, loss of neurotrophic factors, glutamate toxicity, mitochoncrial dysfunction, inflammation
differential diagnosis
secondary Parkinsonism
Parkinson’s plus syndrome
epidemiology
2nd most common neurodegenerative disease (after Alzheimer’s) Incidence rises steeply with age Most common over age 60 1% of people over age 60 4% over age 80 5-10% onset age 20-50 (young onset PD) Higher incidence in Causasians M:F 1.5:1 slightly more common in men 1.2 million people in Europe affected
secondary Parkinsonism
Multiple possible causes: Toxins Carbon monoxide, manganese Structural brain damage Tumour, trauma, hydrocephalus Drugs Neuroleptic drugs, dopamine-depleting agents Infections Post-encephalitis, AIDS, Creutzfeldt-Jakob Disease
parkinson’s plus syndrome
Idiopathic
Includes other syndromes:
Progressive supranuclear palsy (PSP) Multiple system atrophy (MSA) Corticobasal degeneration (CBD) Dementia with Lewy Bodies (DLB)
Beyond the scope of this lecture
diagnostic criteria
No single laboratory test
(Pathological diagnosis based on Lewy bodies in basal ganglia)
Diagnosis based on clinical exam and presence of 2 out of 3 cardinal symptoms of resting tremor, bradykinesia and rigidity
+ Absence of other cause of Parkinsonism
+ Absence of upper motor neurone signs
+ Response to levodopa (clinical improvement 4-8 weeks)
must be given by a neurologist
basal ganglia
Many proposed function Not all related to movement Different nuclei of BG make loop Info from pre motor cortex Impulse to striatum Made up of caudate and putamen Take in signal first Message to output nuclei Output then to thalamus Ventral anterior and ventral lateral nuclei Series of inhibitory loops
Motor plan of body – postural stability plan for standing
To walk – turn off postural control mechanisms and turn on step mechanisms
BG give automatic mechanism ensuring good amplitude movement at the right time
Walking – don’t think about step length
No dopamine – too inhibitied steps are too small
BG not functioning in park –have to use other ways to achieve good movement
excitatory pathways Glutamate Inhibitory pathways GABA Modulatory pathways Dopamine
clinical features
Three cardinal symptoms:
Resting tremor
Bradykinesia
Rigidity
Leading to:
Postural instability and impaired balance reactions
Gait impairment (shuffling, freezing)
Plus many other symptoms and signs
resting tremor
Often first symptom noticed
Occurs at rest, diminishes when hands moved
Frequency 4-6 Hz (slow)
Hands affected first, then legs, chin, mouth, tongue
Often unilateral, may progress to other side
Characteristic: flexion of fingers, rotation of
wrist joint (“pill-rolling”)
bradykinesia
Slowness of movement
Difficulty with repetitive automatic tasks, e.g. writing, walking, playing music
Limbs have decreased amplitude on all movement tasks
Manifestations:
Micrographia
Shuffling gait
Hyphonia
Tests: finger tap tests - tap finger on table at certain amplitude
hand open / close, heel tapping
speaking - quiet tone
feature of the Parkinson’s disease
postural instability
Combined effect of rigidity and bradykinesia
Loss of postural reflexes: anticipatory adjustments and righting reactions
Festination in gait
Also associated with freezing
freezing gait
Sudden inability or hesitancy in moving
limbs during gait
Most commonly in gait initiation and
turns
Once freezing is overcome, movement might be normal (“thawing”)
Falls can occur during freezing episodes
FOG = freezing of gait
non-motor symptoms
Neuropsychiatric: cognitive impairment, depression, anxiety, psychosis (late stage)
Sleep disturbance
Autonomic dysfunctions: hypotension, urinary dysfunction, sweating
Gastrointenstinal: drooling, dysphagia, nausea, constipation
Sensory: olfactory disturbance, pain, paresthesia
Other: fatigue, weight changes
Non-motor and cognitive symptoms indicate that PD is not just a disease of the basal ganglia, but that cortical functions are also impaired
impairments in execute functioning
Internal control of attention
Set shifting: changing attention between one or more stimuli
Planning
Conflict resolution
Concentration
Retaining and using information
Dual task performance
Decision-making (considering advantages and disadvantages of options)
Social interaction (understanding others’ intentions, desires and humour)
Consider the implications for physiotherapy.
imaging
MRI and CT no useful
PET studies demonstrate reduced uptake in striatum SPECT can quantitatively measure dopamine in basal ganglia
medical management
The goal is to replace Dopamine (DA)
Levodopa = precursor of DA
Converts to DA once it crosses BBB by dopa decarboyxlase (DDC)
Combined with DDC inhibitors to prevent conversion in peripheral tissues
Sinemet = levodopa + carbidopa Madopar = levodopa + benserazide
Gradual introduction of L-Dopa
Maintenance dose 300-600 mg / day
Marked improvement in rigidity and tremor
Less improvement in gait
Side effects
Gastrointestinal Cardiovascular Psychiatric
Half life = 1.5 hours
Best effect after 20-30 mins, can last 8 hours
problems with L-dopa
Effectiveness decreases over time
“End-of-dose” deterioration: worsening of motor symptoms before next dose due
Morning dystonia, nocturnal akinesia
Dyskinesias emerge in 50% after 5 years
other medication
Dopamine agonists Apomorphine, rigotine, pramipexole More side effects than L-dopa Delay dyskinesias COMT inhibitors Catecholamine-O-Methyltransferase Adjunctive with L-dopa Monoamine Oxidase B Inhibitors Anticholingergics Amantadine
surgical treatment
Considered where limits of medication are reached: worsening, non-responsive symptoms
Neurosurgical options: Thalamotomy Pallidotomy
Deep brain stimulation (DBS)
assessment
observation Posture Speech, saliva management Tremor Facial expression
posture and gait Flexion
Shuffling
Freezing
TUG
movement
tone
ROM
strength
gait feature
Slowness of movement Difficulty with gait initiation Temporal-spatial changes: Uneven step lengths Slow speed Reduced cadence Increased double support time Kinematic changes: Flexed hips and knees Reduced angular displacement hips / knees / ankles Reduced arm swing Reduced foot clearance
destination
freezing
falls
PD symptoms affected by
Constipation Illness / surgery Stress episode Dehydration Withdrawal / medication change / non compliance Use of contraindicated medications (neuroleptics) Depression Pain Anxiety, panic attacks Poor sleep
goals of physio
maximise
independence
safety
function
maintain or improve Prevent deconditioning
Maintain strength
Manage bradykinesia, rigidity Reduce falls
Maintain flexibility
Optimise gait
Improve gross motor coordination Maintain balance
core areas of physio
gait
transfers
posture
balance
exercise
strengthen
CV
balance
cognitive movement strategies
cueing
Tf training
LSVT -BIG
neuroplasticity
Process of encoding experience in the brain and learning new behaviour through modification of synapses
Exercise
Planned, structured and repetitive physical activity for the purposes of conditioning any part of the body
motor learning
practice to induce a relatively permanent change in motor performance and skill
strengthening
weakness in PD
limbs: quads hams DF PF
axial rest swallow and pelvic floor
resistance training is effective in PD in improving mobility improving strength and is safe
Under-dosing is the standard of care
Concentric then eccentric
Intensity:
60-70% 1RM, 8-12 reps x 3 sets
6-12 sessions then load increased
Frequency 2-3 times per week
Duration 8-16 weeks
aerobic training
Counteract decreased physical activity
Increase exercise capacity can perform more vigorous activity
Increase exercise efficiency can perform everyday activities with less effort
Possible cognitive benefits
Potential to decrease cardiovascular risk profile
Possible other non-motor benefits (improve sleep, reduce depression and fatigue)
Potential for neuroplasticity
cues
Off L-dopa: generalised reduction in movement amplitude
On L-dopa + cues: marked increase in movement at all joints
Evidence for mismatch between cortically selected movement amplitude & actual size of movement due to defective basal ganglia output to SMA & pre-motor cortex
Overcome by cues which use a different input system (visual or auditory)
RESCUE trial by Neiuwboer (2007)
Cues in the home environment
Significant improvements in gait speed, step length, freezing (only in freezers), falls efficacy
Limitations: Carryover can be low, may need permanent cueing devices Considerations:
Identify the best cue: visual or auditory, and tempo / rhythm
How to implement: headphones (outdoors – safety), music
key points for PT RX
Exercise capacity can be increased with judicious exercise prescription in mild – moderate PD
Strength training: Underdosing is the standard of care
Cardiovascular training: Consider trade-off between intensity and duration
Always exercise “on” medication
Consider non-motor symptoms and individual preferences
Monitor with HR or RPE
exercise options for Parkinson’s
CV - cycling walking treadmills +/- cues dancing boxing tai chi functional activities LSVT BIG PRE strengthening movement
movement strategies
Cognitive
Use intact frontal cortex: think things through
Conscious performance of sub-movements
Conscious planning and ending of movement execution Practicing sequences
Attentional movement strategies Conscious attention
Part practice
Mental rehearsal
cognitive movement strategies
Sitting Down
Approach the chair with firm steps, at good pace
Make a wide turn in front of the chair and stop straight in front of the chair. You must have the feeling that you walk around something first (first, practise this, for example, with a cone in front of the chair, later without the cone. If necessary, turn at the rhythm of the cue you already used when you were approaching the chair)
Place your calf or back of the knee against the seat
Bend slightly forward and bend through the knees, keep your weight
well above your feet
Move with your hands towards the arms of the chair or the seat, seek for support with your arms
Lower yourself in a controlled manner. Sit down well, at the back of the
chair.
dual tasking
Often a trigger for freezing
Deficits in planning of movement Inability to produce and time force
Example: draw a triangle while squeezing a ball with your other hand
Dual task training when walking is effective in improving step length (Brauer, Morris 2010)
Increase dual tasks in difficulty
transfers
roll in bed lie to sit sit to stand onto floor back up in and out of car
training
cog movement strategies
reps and practice
aids
bed rail
rise recliner
raised toilet seat
MSK changes
Think of posture: which muscles are in a shortened position?
Stretch flexors (gastrocs, hamstrings, hip flexors)
Prone lying
Thoracic / cervical spine and shoulder girdle
BIG exercise strategies
family and MDT
Patient and caregiver education Support group Occupational therapy Speech and language therapy Diet and nutrition Psychosocial interventions
later stages
Hoehn and Yahr Stage IV and V: limited mobility
Physiotherapy goals and management move towards Maintain
and Prevent
Continue to manage mobility and maintain activity, e.g. chair- based exercises, active-passive trainers, assisted standing, sitting out
Prevent pressure sores and contractures
Respiratory management (saliva)
Palliative care principles and practice may apply
Support the patient, family and carers
