Parkinson's disease Flashcards

1
Q

define parkinsons

A

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

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2
Q

aetiology

A

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

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3
Q

differential diagnosis

A

secondary Parkinsonism

Parkinson’s plus syndrome

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4
Q

epidemiology

A
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
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5
Q

secondary Parkinsonism

A
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
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6
Q

parkinson’s plus syndrome

A

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

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7
Q

diagnostic criteria

A

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

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8
Q

basal ganglia

A
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
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9
Q

clinical features

A

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

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10
Q

resting tremor

A

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”)

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11
Q

bradykinesia

A

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

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12
Q

postural instability

A

Combined effect of rigidity and bradykinesia

Loss of postural reflexes: anticipatory adjustments and righting reactions

Festination in gait

Also associated with freezing

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13
Q

freezing gait

A

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

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14
Q

non-motor symptoms

A

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

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15
Q

impairments in execute functioning

A

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.

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16
Q

imaging

A

MRI and CT no useful

PET studies demonstrate reduced uptake in striatum SPECT can quantitatively measure dopamine in basal ganglia

17
Q

medical management

A

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

18
Q

problems with L-dopa

A

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

19
Q

other medication

A
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
20
Q

surgical treatment

A

Considered where limits of medication are reached: worsening, non-responsive symptoms

Neurosurgical options: Thalamotomy Pallidotomy
Deep brain stimulation (DBS)

21
Q

assessment

A
observation Posture
Speech, saliva
management
Tremor
Facial expression

posture and gait Flexion
Shuffling
Freezing
TUG

movement
tone
ROM
strength

22
Q

gait feature

A
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

23
Q

PD symptoms affected by

A
Constipation
Illness / surgery
Stress episode
Dehydration
Withdrawal / medication change / non compliance
Use of contraindicated medications (neuroleptics)
Depression
Pain
Anxiety, panic attacks
Poor sleep
24
Q

goals of physio

A

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

25
Q

core areas of physio

A

gait
transfers
posture
balance

exercise
strengthen
CV
balance

cognitive movement strategies
cueing
Tf training
LSVT -BIG

26
Q

neuroplasticity

A

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

27
Q

strengthening

A

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

28
Q

aerobic training

A

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

29
Q

cues

A

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

30
Q

key points for PT RX

A

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

31
Q

exercise options for Parkinson’s

A
CV - cycling walking treadmills +/- cues 
dancing 
boxing 
tai chi 
functional activities 
LSVT BIG 
PRE 
strengthening 
movement
32
Q

movement strategies

A

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

33
Q

cognitive movement strategies

A

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.

34
Q

dual tasking

A

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

35
Q

transfers

A
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

36
Q

MSK changes

A

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

37
Q

family and MDT

A
Patient and caregiver education
Support group
Occupational therapy
Speech and language therapy
Diet and nutrition
Psychosocial interventions
38
Q

later stages

A

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