Parkinsons

Question 1

General facts and information -

Answer 1

Second most common neurodegenerative disorder
Indcidence in 1.5 times higher in men than women

Question 2

Parkinsonisms -

Idiopathic Parkinson’s - (definition)

Answer 2

Parkinsonism is the umbrella term that relates to a lot of the different disease processes

Idiopathic Parkinson’s - a chronic, progressive, neurodegenerative disorder resulting from the degeneration of dopamine producing neurones in the substantia nigra of the basal ganglia

Question 3

Risk factors -

Answer 3

Environmental and genetic
Positive association between PD and pesticides
In 5-10% of people with Parkinson’s genetic mutations are responsible.

Question 4

Parkinson’s diagnosis -

Clinical criteria -

Answer 4

PD can only be diagnosed with 100% certainty via a post-mortem brain examination
Criteria:
Bradykinesia - slowness of movement
Diadodyskinesia - reduced speed and amplitude of movements
Rigidity - increased tone. Multidirectional and not velocity dependant
Resting tremor - at rest only, pill rolling tremor
Postural instability
Response to dopamine
Replacement therapy
MRI (supportive only) - specifically on basal ganglia

Question 5

Cardinal signs of PD! -

Answer 5

4 key things that all patients exhibit
Bradykinesia
Rigidity
Resting tremor
Postural instability

Question 6

Secondary clinical symptoms -

Answer 6

Difficulty initiating and terminating movement
Fatigue
Freezing
‘Festinating’ gait pattern - shuffling, flexed posture, generally with no heel strike.
Sleep disorders
Swallow dysfunction (dysphagia)
Anxiety and depression

Each individual will be affected differently with different symptoms

Question 7

What is the function of the basal ganglia?

Answer 7

Well-learned motor skills and movement sequences
Preparation and planning
Initiation and termination of movement
Sequencing and timing
Regulating muscle tone and inhibition of antagonistic/unnecessary movements

Question 8

The basal ganglia, nuclei
Output nuclei -

Answer 8

Globus pallidus - internus and externus
Substantia nigra - made up of pars compacta and pars reticulata

Question 9

The basal ganglia

Input nuclei -

Answer 9

Caudate
Putamen
These both make up the striatum

Subthalamic nuclei

Question 10

Basal ganglia and the cortex -

Answer 10

Basal ganglia receives info from the cortex
Sends information to the thalamus
Which in turn sends information back to cortex

This is the basal ganglia influences movement

Question 11

Basal ganglia pathways
Direct -

Answer 11

Direct pathway promotes movement - go pathway
Cortex sends out excitatory signals to striatum
Striatum ONLY sends inhibitory.. sends to GPi and SNpr
These normally send inhibitory to the thalamus, but because they are being inhibited they don’t
Therefore thalamus sends more excitation to cortex, therefore more movement

Question 12

Basal ganglia pathways
Indirect -

Answer 12

Indirect pathway inhibits movement - stop pathway
Cortex sends excitatory signals to striatum Striatum ONLY only inhibitory.. sends to GPe.
GPe norm sends inhibitory, but cannot as its being inhibited
Therefore cortex sends excitatory to STN as well
STN sends excitatory to GPi and SNpr
There send inhibitory to thalamus
This inhibition stops excitation back to cortex, therefore there is less movement

Question 13

Remember:
Excitation of excitatory nucleus =
Inhibition of excitatory nucleus =

Excitation of inhibitory nucleus =
Inhibition of inhibitory nucleus =

Answer 13

More excitation
Less excitation

More inhibition
Less inhibition

Question 14

Dopamines role -
Therefore with PD -

Answer 14

Dopamine excites the direct pathway
And it also inhibits the indirect pathway
Therefore meaning dopamine promotes movement

Therefore PD, lack of dopamine
Less excitation of direct pathway
Less inhibition of indirect pathway
Ie. Less go and more stop
Lack of dopamine results in lack of movement

Question 15

Medication
Dopamine replacements -

Answer 15

Aims to replace the lost dopamine BUT dopamine cannot cross the blood/brain barrier so these meds all contain drugs that facilitate the crossing to the brain. Eg madopar, sinemet

Question 16

Medication
Dopamine copycats -

Answer 16

Known as dopamine agonists eg apomorphine, pergolide

Question 17

Medication
Dopamine protectors -

Answer 17

Protect the current levels of dopamine by blocking enzymes that break it down
Eg monoamine oxidase B (MAO-B) inhibitors (eg. Selegiline) and COMT-inhibitors (eg. Entacapone)

Question 18

Secondary effects of medication and how they can be managed -

Answer 18

Varied and wide ranging, esp when considering variety of meds people end up taking

Treatment for secondary effects
- deep brain stimulation - treatment generally used to decreased symptoms of dyskinesia which occur as a secondary effect from prolonged dopaminergic treatments
- sitmulation of the STN using electrode input - only used for specific people with advanced Parkinson’s

Question 19

Postural instability -

Answer 19

Develops later in the disease
Characteristic flexed posture
Flexed hips and knees
Unable to access balance reactions

Question 20

Disease progression -

Answer 20

More symptoms
More difficult to manage with medication

Question 21

What is staging?
Tools -

Answer 21

Used to identify disease progression
Clinical staging tools
-modified Hoehn and Yahr scale - quick and easy to administer
Scale 1-5

Research staging tools
-UPDRS - done more in research
Comprehensive but time consuming to complete

Question 22

Principles for enhancing function for PD patients -

Answer 22

Cueing
Duel tasking
Balance training
Gait re-education
Symptom specific training

Question 23

Exercise for PD patients -

Answer 23

Exercise shown to improve function
Pilates
Yoga
Dance
PD warrior

Question 24

Resources for PD information -

Answer 24

Parkinson’s UK
Lip drop Parkinson’s scale
EU Parkinson’s scale
EU Parkinson’s guidelines
NICE guidelines
PD warrior

Question 25

What is dopamine? Main source:

Answer 25

Dopamine is a feel good neurotransmitter The substantia nigra is the main source of dopamine

Question 26

Classifying Parkinsonism into 3 categories -

Answer 26

Signs and symptoms observed in PD, but not necessarily due to PD Primary type of hypokinetic movement disorder 3 types - primary Parkinsonism (idiopathic Parkinson’s disease) -parkinsons plus syndrome -secondary Parkinsonism

Question 27

What is cueing?

Answer 27

Type of treatment technique that uses visual, auditory or kinaesthetic feedback to allow a movement pattern to be accessed and used in a functional way

Question 28

Principles of cueing What ares in brain are we interested in and why?

Answer 28

1) supplementary motor area (SMA) - involved in internally generated, automatic movement 2) pre motor area (PMA) - involved in sensory guided movement - voluntary action In PD, the SMA system is impaired, but the PMS system remains in tact Therefore - automatic subconscious basis of posture and movement is lost (SMA), but abnormalities can often be overcome by voluntary effort (use of PMA) Clinically this means that we incorporate the use of external cues as a coping strategy in treatment

Question 29

How can we cue? 3 main ones -

Answer 29

Auditory - count the patient in/count their steps as they go Music can be beneficial because patient can follow the beat Visual - eg lines on the floor, get them to step over the line Kinaesthetic - move with them Eg rock them to help them stand up or move their pelvis as they walk

Question 30

Downside of PD medications -

Answer 30

Come with a lot of side effects that only get worse the longer you are on them They do not stop disease progression Medications have to be taken at the exact time they are required, they cannot be late Being late may cause them to wear off PD patients have ‘on’ and ‘off’ times during the day where symptoms are either less or more significant.

Question 31

Medications Levodopa, how it works and side effects-

Answer 31

Building blocks of dopamine Taken with another med in order to cross blood brain barrier Becomes less effective overtime Dyskinesias, confusion, hallucinations and delusions, mood swings, psychological changes Sleepiness, fainting or dizziness

Question 32

Medications Mooamine oxidase, type B inhibitor - how it works and side effects -

Answer 32

Reduce fluctuations in effective nets of drugs when have been on them for long periods of time Inhibits action of monoamine oxidase that breaks down dopamine Dyskinesia, headache, aching joints, indigestion, flu-like symptoms, depression

Question 33

Medications Dopamine agonists, how they work and side effects -

Answer 33

Acts in same way as dopamine Can be taken with dopamine and can reduce side effects Nausea, vomiting, constipation, headaches Drowsiness, dizziness or fainting due to low BP Hallucinations Confusion Dyskinesia

Question 34

Medications COMT inhibitors, how they work and side effects -

Answer 34

Block an enzymes that breaks down dopamine down dopamine. Reduces the ‘off’ time Taken with dopamine Dyskineasia nausea and vomiting