Parkinsons Flashcards
General facts and information -
Second most common neurodegenerative disorder
Indcidence in 1.5 times higher in men than women
Parkinsonisms -
Idiopathic Parkinson’s - (definition)
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
Risk factors -
Environmental and genetic
Positive association between PD and pesticides
In 5-10% of people with Parkinson’s genetic mutations are responsible.
Parkinson’s diagnosis -
Clinical criteria -
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
Cardinal signs of PD! -
4 key things that all patients exhibit
Bradykinesia
Rigidity
Resting tremor
Postural instability
Secondary clinical symptoms -
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
What is the function of the basal ganglia?
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
The basal ganglia, nuclei
Output nuclei -
Globus pallidus - internus and externus
Substantia nigra - made up of pars compacta and pars reticulata
The basal ganglia
Input nuclei -
Caudate
Putamen
These both make up the striatum
Subthalamic nuclei
Basal ganglia and the cortex -
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
Basal ganglia pathways
Direct -
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
Basal ganglia pathways
Indirect -
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
Remember:
Excitation of excitatory nucleus =
Inhibition of excitatory nucleus =
Excitation of inhibitory nucleus =
Inhibition of inhibitory nucleus =
More excitation
Less excitation
More inhibition
Less inhibition
Dopamines role -
Therefore with PD -
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
Medication
Dopamine replacements -
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
Medication
Dopamine copycats -
Known as dopamine agonists eg apomorphine, pergolide
Medication
Dopamine protectors -
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)
Secondary effects of medication and how they can be managed -
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
Postural instability -
Develops later in the disease
Characteristic flexed posture
Flexed hips and knees
Unable to access balance reactions
Disease progression -
More symptoms
More difficult to manage with medication
What is staging?
Tools -
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
Principles for enhancing function for PD patients -
Cueing
Duel tasking
Balance training
Gait re-education
Symptom specific training
Exercise for PD patients -
Exercise shown to improve function
Pilates
Yoga
Dance
PD warrior
Resources for PD information -
Parkinson’s UK
Lip drop Parkinson’s scale
EU Parkinson’s scale
EU Parkinson’s guidelines
NICE guidelines
PD warrior
What is dopamine?
Main source:
Dopamine is a feel good neurotransmitter
The substantia nigra is the main source of dopamine
Classifying Parkinsonism into 3 categories -
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
What is cueing?
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
Principles of cueing
What ares in brain are we interested in and why?
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
How can we cue? 3 main ones -
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
Downside of PD medications -
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.
Medications
Levodopa, how it works and side effects-
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
Medications
Mooamine oxidase, type B inhibitor - how it works and side effects -
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
Medications
Dopamine agonists, how they work and side effects -
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
Medications
COMT inhibitors, how they work and side effects -
Block an enzymes that breaks down dopamine down dopamine. Reduces the ‘off’ time
Taken with dopamine
Dyskineasia nausea and vomiting
